| 00:14 | mhm. Hey folks, let's go and get started. So um to |
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| 00:40 | down here um Today we'll finish up 24 and then um 25 on Monday |
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| 00:50 | be basically like a flipped class, bunch of questions and a number of |
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| 00:55 | bigger questions. We'll just center the around around the questions. Um and |
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| 01:00 | 25 is uh so after having gone today, we will have completed basic |
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| 01:07 | at all the different mechanisms and ways your body can fight infectious disease. |
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| 01:12 | then in 25 you're basically just kind looking at the perspective of the |
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| 01:17 | all the ways it can exploit. around and around your chemical barriers, |
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| 01:24 | barriers um and um and others and adaptive immune system. And uh because |
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| 01:34 | there's many pathogens that are successful at , that's why they can cause |
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| 01:38 | And so they've evolved ways to Get these barriers. So we'll look at |
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| 01:44 | Monday. Okay. And then 26 really just kind of One of those |
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| 01:49 | of putting it all together 2°, looking different infectious diseases and we'll bring up |
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| 01:55 | factors and that relate to those diseases defenses you have that relate to those |
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| 02:02 | and so it'll kind of mixed Okay. Um so uh recall there's |
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| 02:09 | couple of things, Do we have work? It's time to do the |
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| 02:14 | . Um Weekly quiz opens tomorrow at . Um It was covered what we've |
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| 02:21 | go through today. So basically the half of 23 and then the rest |
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| 02:25 | 24 include, we'll have a little of uh your book. Does't go |
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| 02:30 | a lot about vaccines, and I'm kind of giving just like an overview |
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| 02:36 | it. Just kind of different types are out there. Um And so |
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| 02:41 | tables that are in there, you need necessarily to memorize those, but |
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| 02:44 | more like if you see the term attenuated vaccine, you know what that |
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| 02:49 | , or you see a subunit you know what that is. So |
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| 02:52 | kind of more more kind of the of different types of vaccines. And |
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| 02:56 | look at the covid vaccines as Okay, so um so uh is |
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| 03:04 | any questions about anything you can That's something administrative stuff I had. |
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| 03:09 | uh remember I think the I didn't it on here, but the the |
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| 03:19 | , for example, for I think supposed to be up on the |
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| 03:23 | so keep an eye out for Um Anyway, so let's look at |
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| 03:30 | first question. So let's start with questions that's going to relate to something |
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| 03:33 | talked about last time. Probably a things we didn't talk about yet, |
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| 03:38 | we'll get into today. Um So of the following is false concerning the |
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| 03:44 | immune response. So, remember last we looked at, here's the overview |
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| 03:50 | the adaptive immune system. Here's what part does. Here's what the other |
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| 03:54 | does. We'll get into a little specifics today. Okay. Okay. |
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| 04:55 | let's sing. So c. Is correct choice? So that's uh look |
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| 05:13 | these others. So be salty. function that's how they differentiate it. |
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| 05:18 | human immunity is the antibody production Uh Sailor immunity is different types of |
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| 05:25 | cells. Certain types interact with your cells that may be infected but t |
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| 05:30 | also are important for activating B cells well. So we'll see how that |
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| 05:35 | . Um B cells of course can into plasma cells. And plasma cells |
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| 05:40 | the ones that form antibodies that can form memory cells. There's two cell |
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| 05:44 | that can be formed by activating B um T cells as mentioned. They |
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| 05:52 | the part of your adaptive immune system can deal with infected cells. And |
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| 05:57 | there's specific t cells that do that cells can produce antibody but B cells |
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| 06:03 | don't really kill anything. Okay. they can through antibodies in their surface |
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| 06:10 | . I'm sorry, anybody's in their . Combined energy and of course multiple |
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| 06:15 | . So but single clonal populations, way that B cells this uh concept |
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| 06:20 | clonal selection. Okay so a population B cells will respond to an energon |
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| 06:29 | uh then there's be self antibodies specific that antigen. Okay so um obviously |
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| 06:36 | key word here is clonal population there going to produce antibodies of the same |
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| 06:42 | that we're buying into the same Okay that's how you're B cells |
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| 06:48 | Okay so we'll go into some of specifics here. So last time uh |
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| 06:53 | so we looked at the overview of of the adaptive immune system. Uh |
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| 06:57 | get into more of how these things . I'm giving you I guess you |
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| 07:03 | the watered down version because um this a very complicated process and though interesting |
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| 07:11 | very complicated. And so uh if do find it of interest you might |
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| 07:17 | taking, we offer an immunology course every other semester I believe. So |
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| 07:23 | might video get all the gritty details the process but um nevertheless so I'm |
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| 07:31 | you more like a Basic 101 version . So just know that even in |
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| 07:37 | of the t cells you see I'm only really mentioning three types. |
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| 07:42 | more than that. Um And we mentioned that B cells of course we |
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| 07:48 | for memory cells but there's also T that can do this. There's also |
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| 07:52 | memory cells as well. So um again I was trying not to get |
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| 07:57 | bogged down into this and just kind give you the basics here. Um |
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| 08:02 | so one of the things I remember that, and not mention this again |
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| 08:06 | that your t cell types. They their functions based on the type of |
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| 08:14 | uh self engines that they recognize that , that kind of what is what |
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| 08:19 | them. And then another differentiation is types that work with macrophages and dendritic |
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| 08:26 | and those that work with B Okay. Um so let's uh see |
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| 08:33 | else we talked about. We talked an engine and body binding and I |
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| 08:36 | remember the epic Toby is a smaller within the engine is actually at the |
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| 08:42 | where the actual physical binding occurs. . And of course engines can be |
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| 08:47 | different things. Right. I guess could loosely defined as an engine is |
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| 08:52 | anything that can stimulate the immune system can be a number of different |
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| 08:56 | Okay. And so with anybody structure so again that Y shaped but of |
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| 09:03 | in multiple subunits um it's it's a obviously it's uh you can have of |
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| 09:09 | multiple if you have five different isotopes by what is the constant region uh |
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| 09:19 | amino acid sequence there. So all the same maestra type will have the |
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| 09:24 | sequences here. They will differ they differ in their image and binding |
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| 09:29 | Okay. But even that you're identifying by the fact that it they all |
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| 09:34 | this same sequence in this constant Right? Which will differ from |
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| 09:40 | Or D. Which will differ in regions. Okay. Um But again |
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| 09:45 | within a media type, right. can have the same or different engine |
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| 09:51 | sites. All right. Um And lastly the effective and anybody buying |
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| 09:57 | Okay. Very defects dealing also with parasites as we see down here. |
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| 10:07 | so um so let's look at uh this is a little bit about the |
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| 10:13 | antibodies themselves. Okay so and the you see here are the proportions that |
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| 10:21 | exist in in the circulating blood. so 15% for Ij IJ mainly resides |
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| 10:27 | the mucus secretions. So I remember your um the mucus membrane is a |
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| 10:34 | barrier and it produces a chemical barrier well. And in because secretions will |
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| 10:39 | a number of different chemicals among them be I. G. A. |
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| 10:44 | and so a lot of your respiratory both bacterial and viral uh rely on |
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| 10:52 | to uh the agricultural surface of your uh system which I'm um and and |
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| 11:01 | idea and embodies to those pathogens can them from binding they produce the neutralizing |
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| 11:07 | antibodies that will quote the pathogen and that doesn't allow them to stick to |
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| 11:13 | cells. Okay now unique with the is that they can form These dime |
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| 11:19 | so um which basically doubles the number binding sites. So we're from 2-4 |
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| 11:24 | that case. Okay um the I . G. Is I call this |
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| 11:34 | of the workhorse antibody. It has functions from optimization to uh acting is |
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| 11:45 | antibodies as well as the activity compliment other functions. Okay it is the |
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| 11:51 | that is formed in the highest amounts as you might say the most |
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| 11:59 | Okay um one of the things that don't go into it but if you |
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| 12:06 | go into it? Your book talks little bit about it is with your |
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| 12:10 | immune system. There's actually a learning so to speak for your antibody producing |
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| 12:18 | that the antibodies initially um will bind antigen but not as tightly. But |
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| 12:26 | get better at it with prolonged exposure an urgent and so the next generation |
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| 12:31 | antibodies synthesized following the initial exposure to better at binding. And so they |
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| 12:38 | they become better in there in terms their engine antibody activity. Okay. |
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| 12:44 | it's those high Gs that are formed first exposure to the vaccine. Those |
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| 12:51 | in high amounts and are very bind well initially it's I. GMOs that |
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| 12:56 | pretty much the Gm antibodies that don't as well. But they kind of |
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| 13:04 | by being able to form those these five headed monsters. It's a it's |
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| 13:08 | pen timer. Okay getting ahead of . I'll show you that that's what |
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| 13:11 | talking about. Let me just go . I'll come back to that. |
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| 13:14 | so here's I. G. So it can form A. Um |
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| 13:18 | A. And M. Can also in the monomer, the singular Y |
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| 13:22 | . But they can also they also these and for I. G. |
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| 13:25 | . S. This is an effective to kind of compensate maybe for not |
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| 13:29 | very good at binding but they combined units so to speak. The unit |
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| 13:35 | a pattern let's say okay so Who reducing the number of infectious units that's |
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| 13:40 | illumination the clumping function. Right. so by having now 10 binding sites |
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| 13:46 | can reduce the number of units infectious the body has to deal with. |
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| 13:50 | so that's that's a good function. these are what are produced early on |
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| 13:54 | first exposure to engine are these types then switch over to A. |
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| 13:59 | G. Which are better binding and higher quantities. Okay so let's go |
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| 14:06 | to here. And so these are took only 10%. Don't worry so |
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| 14:11 | about the values uh the I. . G. S. Are in |
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| 14:15 | highest amount in the circulating blood. Sit back here step so there's a |
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| 14:24 | of antibody types and let me just you probably notice anyway. But the |
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| 14:29 | I. G. B. G. In front of these |
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| 14:31 | So it's um you know just a name for antibody right means the same |
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| 14:35 | . Um .2%. So there's a of types i. g. |
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| 14:41 | and i. g. e. do their work while sitting on top |
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| 14:46 | the cell. Okay. And D. And B. Cells which |
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| 14:50 | antibodies we'll have actually either I. . D. On them. |
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| 14:55 | Or the I. G. Modern reforms. Okay secondhand one. |
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| 15:02 | can be D. Or mm. and that's how B cells can interact |
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| 15:10 | . And even though they can also engulf an urgent and present antigen. |
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| 15:15 | ? So they'll be able to show but that they can show it right |
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| 15:21 | because they have MHC Type two molecules they can show hands again um Using |
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| 15:29 | . Okay. And they do. another type of mm hmm. Of |
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| 15:34 | two types of ways of activating B and this is one of them to |
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| 15:38 | antigen so that it can it can a T. Cell help it out |
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| 15:42 | activate it. That's correct. Ah anyway so I. G. |
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| 15:47 | Uh is one that sits on top uh antigen and are found on B |
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| 15:54 | . Okay so because they're so they're low in the blood because or your |
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| 15:58 | cells your T. Cells your Dendritic cells as their primary residence is |
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| 16:05 | fluid. Not not being in your so much. Okay. And so |
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| 16:10 | that's where you'll find I. D. S. With B cells |
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| 16:12 | are in lymphatic. Okay. Or tissue. Um They just talked about |
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| 16:18 | . G. M. S. I. G. E. Okay |
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| 16:21 | I. G. E. Another found on not on the stones but |
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| 16:25 | found on mass cells battlefields. We these types in the inflammatory response. |
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| 16:33 | these are about releasing cytokines which have effects. Um And so I. |
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| 16:39 | . S. Will bind antigens and cause these effects um also those of |
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| 16:46 | that suffer allergies. Um this will lead to that. Especially if you're |
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| 16:52 | you'll produce more than than what other do. And then that leads to |
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| 16:57 | usual symptoms. Watery eyes uh itchiness. Maybe these kind of symptoms |
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| 17:04 | experience from allergy because the and you it doesn't have to be coming from |
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| 17:08 | microbe. That can be a what's the yellow stuff that's out and |
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| 17:13 | Now the oak pollen I think it . That's that's an engine for |
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| 17:17 | Okay so and some of us just more vigorously than others so to |
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| 17:23 | But uh anyway um now so let's any questions about that anybody types. |
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| 17:34 | so uh so how did you make things? So this number can be |
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| 17:38 | at B. Cell function here. humorless response. So remember that anybody's |
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| 17:43 | go inside of a cell and deal an infected cell. They can only |
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| 17:46 | on pageants that are outside. So extra settings are pathogens. Okay so |
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| 17:52 | two processes. There's what's called, you're gonna see here is um um |
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| 17:58 | . Cell dependent so T dependent activation a. B. Cell. Okay |
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| 18:05 | also t independent activation. Okay so what has to happen is the |
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| 18:11 | Cell has to get involved and activate B. Cell. Okay. The |
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| 18:16 | of engines that generally, well not . Well I hesitate to say all |
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| 18:24 | time but for the most part protein are what goes through this process. |
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| 18:30 | most engines that are out there are in nature. Okay. And so |
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| 18:35 | a reason for that. I'll explain little bit. So anyway so an |
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| 18:41 | again will bind to antibodies on the cell. Typically D. D. |
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| 18:47 | . G. D. Or G. M. And um those |
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| 18:51 | will be in the process of It doesn't mean it's activated but that's |
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| 18:55 | like step one. Okay. MR and then as well being an engine |
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| 19:02 | cell remember B cells macrophages, dendritic and present. They will do that |
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| 19:08 | and show it to a T Okay. And so t cell binding |
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| 19:14 | basically the next step. Okay. uh it then that causes it to |
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| 19:20 | cytokines, cytokines among those are chemicals will activate the B cells to differentiate |
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| 19:27 | plasma cells which directly form antibodies And cells. Okay so memory cells don't |
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| 19:35 | antibodies. Okay. But they do respond to an urgent uh and they'll |
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| 19:41 | primed and ready to they buy an very quickly. They differentiate into plasma |
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| 19:48 | and more memory cells. Okay. now the the process of this clonal |
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| 19:58 | . Okay so um so we have have in terms of numbers um numbers |
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| 20:10 | but you obviously have many B cell of cells in your body and B |
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| 20:17 | are unique. So most of the almost all the cells in your body |
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| 20:22 | course are genetically identical or in the chromosomes the same D. N. |
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| 20:27 | . Um the B cells as But the B cells have visibility. |
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| 20:32 | have a segment in their chromosome which part of the antibody production process. |
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| 20:39 | they can produce remember the the energy sites. Right? That's the part |
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| 20:46 | variable in an antibody. And so B cell can produce can can have |
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| 20:51 | recombination events occur in this region that these and combining sites. And so |
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| 20:58 | been thought that there's like potentially 10 the 13 different kamen unique engines can |
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| 21:03 | recognized. 10 to 13. That's lot. Okay so you can form |
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| 21:09 | up these cells that formed antibodies realistically almost anything that you might encounter for |
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| 21:15 | reason. So you're gonna have these of antibodies and so forth. For |
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| 21:21 | it simple. The it's just showing four different subsets of B cells that |
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| 21:27 | might have. Okay but only one them is going to respond to the |
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| 21:32 | . Okay that's that this this process clonal selection. Okay so the term |
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| 21:39 | uh antigen. Okay so for four . Four. So here's red dots |
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| 21:45 | the engine and four C. Is one that actually binds them and then |
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| 21:51 | . Okay so for four C. whatever it is is it's cognitive and |
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| 21:58 | for 32 or one it would be different. Okay and so the binding |
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| 22:04 | initiates this proliferation of of clones that of this particular type. So B |
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| 22:12 | will then proliferate and the antibodies on of these cells will only bind to |
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| 22:19 | specific episode. Right? That's shown . Okay. And so um again |
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| 22:26 | become platinum sells some become memory Okay. And this is the this |
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| 22:31 | still India under the umbrella of of dependent activation of the B cell. |
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| 22:41 | . So um what about this t activation? Okay. These this process |
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| 22:49 | kind of just reserved for certain molecule can induce this. Certain engine types |
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| 22:55 | do this not proteins but rather larger antigens. So called the sacral rides |
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| 23:03 | acids. Um Golightly lipids, large lipids. These are types that can |
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| 23:09 | activated B cell without the help of T. Cell. Hence t independent |
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| 23:15 | . Okay, so the reason for is this And what I'm about to |
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| 23:19 | that you don't just for information we're going to help you understand this. |
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| 23:23 | not gonna test you on it. . In really basic terms what has |
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| 23:28 | happen is what they call, Let just show this picture and there's a |
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| 23:32 | of this I don't like but I'm go with anyway. So uh what |
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| 23:37 | to happen is the formation of a cell receptor. Okay. B. |
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| 23:44 | . R. For short. A. B. C. |
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| 23:48 | Is basically this the antibody bound to cell but then there's a little projection |
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| 23:55 | goes in that enables it to to in the membrane. Alright, so |
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| 24:02 | actually a difference between this and that different only in the fact that these |
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| 24:09 | antibodies that that are floating around and their thing don't have or lacking |
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| 24:15 | I mean they don't have it that pin in portion that allows it to |
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| 24:19 | in the membrane. Okay, this up here is all the same. |
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| 24:24 | , but this is lacking in this . Okay, so um then there's |
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| 24:31 | hey a couple of anybody black molecules here. Okay. And what has |
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| 24:41 | happen is you have to activate the cell and step one is by |
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| 24:47 | Okay so buying the Andersen. Alright then you need to get that signal |
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| 24:58 | it's the nucleus. Okay. And get that signal of that binding signal |
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| 25:05 | to the to the nuclear So then can create the chemical initiate collection of |
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| 25:09 | set of kinds that enable the process be going Okay so it's this kind |
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| 25:15 | sort of doesn't relate to do What you have to do is to |
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| 25:19 | together. You have to cluster together b cell receptors come together. |
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| 25:27 | so a a something like this. these are clustering together. Right. |
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| 25:34 | that's what is part of the activation . Okay, so protein engines. |
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| 25:41 | . Because of their to be able cluster together multiple antibodies in the |
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| 25:46 | Okay, you they have to be contact with a repeating epic tobe right |
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| 25:54 | other words, a molecule that has same epic tope right binding site. |
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| 26:02 | , repeating epitope. Okay, so is the and again, right here |
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| 26:07 | the episode. So these have to repeating, right? Because the antibody |
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| 26:13 | antibody is going to buy into one right? On a single B |
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| 26:16 | So you need to have So if the same and it's big, |
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| 26:22 | Like let me go back real quick this illustration to here. Right. |
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| 26:25 | see how big the engine is. . You can contact always be some |
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| 26:30 | and cluster them together. Right. clustering is what activates this thing over |
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| 26:38 | that sends a signal to the Okay. And then that sets the |
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| 26:42 | the whole chain of events. Um and so a big molecule like |
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| 26:46 | police accurate you know, think of starch. Right? Or or like |
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| 26:52 | just repeating glucose units. Right. are repeating epic taub's right. A |
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| 26:57 | play play peptide is not right because an individual amino acids right. Making |
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| 27:03 | with things. There's a lot of there. Okay, So that's why |
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| 27:08 | you know, you can't really do very well. Okay. And that's |
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| 27:12 | they need the involvement of a T to help the activation. Okay, |
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| 27:17 | a large like a nuclear gas suit place Saccharine. Right. There's not |
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| 27:24 | that same different variability as there is the protein. Right. And so |
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| 27:29 | have that repetition. Okay. And we've got plenty of saccharine or or |
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| 27:34 | acid and and and you have a as well as those things. And |
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| 27:38 | that's what can cause a much easier clustering these these B cell receptors together |
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| 27:45 | then get the signal to the nucleus them begin the activation. Right? |
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| 27:50 | it does not need a T. or so. Okay. And so |
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| 27:55 | that's what's going on. Okay. so this is a little misty I |
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| 27:59 | to correct that the cell receptor this a B cell receptor. That's a |
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| 28:04 | cell receptor. You're trying to cluster together to get the activation right, |
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| 28:09 | for a big place Ackroyd plague acid do that because they're not really they're |
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| 28:14 | repeating units. Right. Protein. so much. Okay. But |
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| 28:20 | the most engines encountered our protein in . And so it's gonna be the |
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| 28:24 | cell activity dependent process that's going to happening in the majority of the |
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| 28:29 | But you do have this occur certainly occasion. But what the sacrifice is |
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| 28:37 | . Okay. Um this this t independent activation suffers from the fact that |
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| 28:45 | you will form um plasma cells okay activate it and form plasma B |
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| 28:54 | Okay. Which of course are the producing cells. All right. But |
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| 28:58 | don't produce memory cells. Okay. what you do by the t the |
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| 29:04 | cell dependent one. Does you get full effect memory cells plasma cells. |
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| 29:10 | . Um But I can't explain the why but but it is that the |
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| 29:16 | it may I'm sure it has something do with the tight binding that proteins |
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| 29:19 | have with their antigens with Yeah Um And so the the as always |
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| 29:32 | tend to be the best engines in of better binding uh followed by |
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| 29:37 | play cigarettes and then take acid. the left knee has something to do |
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| 29:41 | that. But regardless the T dependent t independent process. The bottom one |
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| 29:49 | one where you only police past myself memory cells. Okay. Um Many |
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| 29:56 | about that. Yeah. So what differentiates without it? It again it's |
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| 30:08 | it's about clustering those B. Cell together. Check so a big engine |
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| 30:15 | that. You see how this is together. Yes because they have this |
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| 30:21 | a repeating big repeating molecule. So engine binding sites are gonna recognize that |
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| 30:27 | epitaphs because the episodes are repeating throughout the whole molecule so it will bind |
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| 30:36 | and the size of the molecule the . So it's it's clustering together all |
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| 30:43 | B. Cell receptors to create the . Okay and doesn't need a T |
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| 30:48 | protein engines. I don't really do very well. And so it involves |
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| 30:52 | why you have to involve a Cell. Because the protein engines don't |
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| 30:57 | so much on the clustering they rely the activation by a. T. |
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| 31:02 | . Yeah so it gets cut out middleman. Okay that's when I look |
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| 31:08 | it. But again most of the that occurs of a B. Cell |
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| 31:11 | your body is through T. Cell process because most proteins are the most |
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| 31:17 | protein in nature. Technical. Especially on on pathogens. So how |
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| 31:25 | we be able to identify what is independent? Um Oh the because the |
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| 31:34 | T um independent process is like a place aka rides and nucleic acids too |
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| 31:43 | proteins proteins correct? Pretty much. . Yeah like I said there's there's |
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| 31:51 | exceptions to that but that's pretty much role. Yeah. Right. Any |
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| 31:57 | questions? Okay. Um Like I you might find the immunology fascinating course |
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| 32:05 | you might be pulling your hair out . I don't know. Um Okay |
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| 32:11 | let's look at this question. Let's this into the next part here. |
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| 32:17 | Kind of the stuffing I think you're with I'm sure um Having well I |
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| 32:26 | assume that you've gotten vaccinated but I ask if you got vaccinated but that's |
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| 32:31 | of what the process is here. looking at. Just making a quick |
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| 32:39 | . It's not maximizing. Sure. huh. Uh huh. No I |
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| 32:45 | want to get fired. Okay. yet. Alright, secondary antibody response |
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| 33:11 | antigen it is. Let's see mm . Yeah of course it's going to |
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| 33:27 | memory cells. So um the so the first part here so this can |
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| 33:35 | um first vaccination it can be um exposure. Just an infection. First |
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| 33:44 | to a pathogen that causes an infection you. And the primary response is |
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| 33:49 | to form uh plasma cells. So social activating from plasma cells and memory |
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| 33:59 | . Okay so generally you can see timeframe it's gonna be a little bit |
|
| 34:03 | here versus here for the effect. the second of course secondary secondary responsible |
|
| 34:11 | much quicker because you have memory cells and ready respond to an urgent and |
|
| 34:16 | you can form plasma cells and produce quicker than than first exposure. So |
|
| 34:23 | so just elaborating on that a bit the production of I. G. |
|
| 34:32 | . And I G. Has mentioned initially and again there's this learning curve |
|
| 34:38 | producing stronger antibodies let's say. Um just think it just requires just prolonged |
|
| 34:46 | . The more the more exposure you to the engine I guess the better |
|
| 34:49 | bodies get. Okay. And so B cells will for my Gm initially |
|
| 34:56 | those are the ones that formed those er 55 of those together. Okay |
|
| 35:02 | the illumination function is big there and their fault then those B cells it's |
|
| 35:08 | what's called ice A type switching. they'll go from switch from making M's |
|
| 35:16 | Bodies two GS. But what's kept same is the energy and binding sites |
|
| 35:22 | those have probably gotten better in terms being able to bind to And |
|
| 35:28 | um and so you produce more of as well. So uh m followed |
|
| 35:33 | G at a higher level. And then um the uh second exposure |
|
| 35:42 | you just soften the question of course gonna be much bigger because you have |
|
| 35:46 | bunch of memory B cells ready to following exposure check. So obviously when |
|
| 35:53 | look at um we'll talk a little about vaccines in the bed. Uh |
|
| 35:57 | of course it's all based on on . Okay. And we'll see some |
|
| 36:03 | in terms of vaccines. Um So , so t cells so here we'll |
|
| 36:11 | a little about different T cell types their functions and it really relates to |
|
| 36:16 | type of MHC class they respond Okay, so you started toxic t |
|
| 36:24 | . So let me before I do . So there's also another thing. |
|
| 36:29 | , t cells recognize MHC molecules self and they also recognize antigen. |
|
| 36:40 | so antigen and MHC molecules, that you're gonna have a receptor for |
|
| 36:44 | Okay, so you see here the A C receptor what they're calling a |
|
| 36:51 | cell receptor. Okay. Here which the edge. And then there was |
|
| 36:57 | co receptor and that binds to the molecule type. Okay, so CB |
|
| 37:04 | recognizes self engines. Class one. ones. Cd four core receptor recognizes |
|
| 37:11 | Class two tells you. Ok, class type recognized, Told you |
|
| 37:17 | what kind of cells to interact Right, so, you remember class |
|
| 37:20 | or what you see there macrophages? cells and B cells. So these |
|
| 37:24 | up being what we call T helper sub h. How we designate them |
|
| 37:32 | and two. Okay. And the interact with B cells, the ones |
|
| 37:41 | macrophages and dendritic cells. And of , and this is only one type |
|
| 37:47 | here, side of toxic T And so recognizing self engine type |
|
| 37:52 | So, your type ones of are basically all of your body |
|
| 37:55 | right, liver cells, skin etcetera. Okay, so any of |
|
| 38:00 | cells that potentially get infected virus or then? Uh potentially they could be |
|
| 38:06 | out by um side of toxic T . Okay. Um so let's look |
|
| 38:13 | little closer at that. So, what we call cell mediated immunity ah |
|
| 38:21 | these these T cells interact specifically with cell types. Okay. And create |
|
| 38:26 | effects. And so dealing with intracellular , of course, right infected cells |
|
| 38:33 | again, it's not necessarily doesn't apply every virus infected cell and may vary |
|
| 38:38 | terms of effect. You know, depends on, you know, the |
|
| 38:42 | of the cell that's infected to show . I'm guessing there are times maybe |
|
| 38:48 | on the viral infection type that it be better or worse at that, |
|
| 38:53 | on the viral type I'm assuming. But nonetheless, uh we all know |
|
| 39:00 | viral infection are approaches were made, have to assemble and so forth. |
|
| 39:04 | during that process and then they receive made money affect itself and buy into |
|
| 39:10 | of these viral antigens and bringing to surface. Okay. Um similarly we'll |
|
| 39:18 | this next time. But you know are bacterial types that can do this |
|
| 39:22 | they do it not for the purpose using the cell to replicate but to |
|
| 39:26 | out. And so that may be engines from that can sometimes be uh |
|
| 39:34 | as well. Nonetheless, the point the engines that are shown. They |
|
| 39:38 | potentially be recognized by T cells side toxic T cells. Okay. And |
|
| 39:43 | so that binding will initiate a release chemicals. Some of these chemicals will |
|
| 39:51 | into the membrane much like a We've seen these chemicals before, preference |
|
| 39:58 | natural killer cells. Defense is a . We saw an innate immune |
|
| 40:05 | They kind of act like just puncturing cell membrane. Creative license. They |
|
| 40:10 | can produce chemicals that induce a popped sis remember that's that program cell death |
|
| 40:15 | tells the cell to basically destroy The bottom line is if it's a |
|
| 40:21 | cell of sometime if you want to rid of it running out of population |
|
| 40:24 | obviously a virus infected cell can produce viruses. So you want to get |
|
| 40:29 | , get it taken care of. , so that's what sort of toxic |
|
| 40:33 | cells do. Um so too can killer cells in a little bit different |
|
| 40:38 | . Okay. Not necessarily as specific this but they too can deal with |
|
| 40:43 | in fact itself. Okay so the . Helper cells the type one and |
|
| 40:51 | two. So we talked about this before. Uh this is about activating |
|
| 40:58 | macrophage or dendritic cell using a Helper cell of the type one |
|
| 41:05 | And so these recognize MHC 2s which course are on these cell types |
|
| 41:10 | These engine presenting cells and so again binding leads to um release of |
|
| 41:18 | Okay. And these can um it two ways you'll have cited and released |
|
| 41:24 | the T. Helper cells but also the in this case macrophage. |
|
| 41:30 | And that can lead to further activation more T helper cells uh it will |
|
| 41:37 | this. So remember that activating one these means you are you are creating |
|
| 41:44 | effect over here. We saw this . So here's a resting macrophage and |
|
| 41:49 | are all activated macrophages. So the of membrane folds these little arms sticking |
|
| 41:55 | increases because that potentially can increase the of it to bind and engulf microbes |
|
| 42:02 | enhanced activity. You you want to certainly in the time of an |
|
| 42:06 | So um and so the T. type two as we saw their function |
|
| 42:12 | in the tea T cell dependent b activation. Right? Helping B cells |
|
| 42:19 | activated. Um So many. Not any questions about the cells Yeah it's |
|
| 42:30 | different between t side of France Yes there is because natural killer cells |
|
| 42:36 | not respond to androgen the same Plus I'm doing part of the story |
|
| 42:42 | out here because I'm not trying to too bogged down that side of toxic |
|
| 42:46 | cells can also have memory. They also proliferate and they can produce a |
|
| 42:53 | of them that was brought into the antigen and natural killer cells don't work |
|
| 42:57 | way. Okay. Um They do for so natural killer cells look for |
|
| 43:02 | that lack MHC molecules, so a bit different function and not really looking |
|
| 43:08 | antigen more for kind of like anomalies the membrane that having a lack of |
|
| 43:15 | engines would would be something like Okay. So similar. Maybe similar |
|
| 43:19 | terms of what they look for but similar in terms of how to do |
|
| 43:22 | and how they function. Yeah. . Exactly. Exactly. Yeah. |
|
| 43:32 | right. Exactly. Exactly. Right. Um Okay, so this |
|
| 43:39 | this is actually one thing. It's kind of not that complicated but you're |
|
| 43:43 | your book doesn't mention it really. Let's look at this question here. |
|
| 43:47 | it kind of follows starting here. . And then going down two types |
|
| 43:55 | of adaptive immunity and then there's another alright, active or passive, so |
|
| 44:02 | what do you think would represent Mhm. Which would represent the |
|
| 44:08 | Which would probably be vaccination. Best . Okay if the majority is |
|
| 44:56 | It is c okay so you can what would uh what would ah let |
|
| 45:08 | think. What would a baby a acquiring um everybody's from his or her |
|
| 45:16 | during breastfeeding? Yeah it's naturally required it's not like an active response. |
|
| 45:23 | . Right. Natural part. So have basically four flex. Right? |
|
| 45:28 | basically it's naturally acquired artificially. I we can probably figure that out pretty |
|
| 45:33 | . Right so it's are you getting shot basically? Are you acquiring into |
|
| 45:37 | infection or um uh or passively as mother to the child? Um And |
|
| 45:47 | course the active passive process is is body actively making them or not? |
|
| 45:54 | and so certainly vaccination or infection. ? As a response to an allergen |
|
| 46:01 | you your body is producing those So both of us will be active |
|
| 46:05 | is obviously using a needle is artificially um A passive process. Of course |
|
| 46:11 | not making them. So the baby not making the antibodies but it's receiving |
|
| 46:15 | preformed ones from the mother. Similarly can go you can uh they do |
|
| 46:21 | shots of I think it's I think I. G. Is what they |
|
| 46:25 | give us a shot for various treatments you need. Okay obviously that's artificial |
|
| 46:33 | passive. Okay so um So that's 20. Well not quite because vaccines |
|
| 46:40 | still a part of it but in of the going through B cells and |
|
| 46:45 | cells, et cetera. They questions I move on civil look at some |
|
| 46:50 | of vaccinations. So we know vaccination um having just gone through it. |
|
| 46:57 | probably do this before this class But what you we haven't gone through |
|
| 47:04 | this Okay. So this table. . It's showing you obviously diseases on |
|
| 47:13 | side, infectious diseases of different types what's called an R. Value? |
|
| 47:18 | of the R. O. Is of the reproductive value of the infectious |
|
| 47:23 | . Okay. So if a person infected, how many other people could |
|
| 47:31 | that he or she potentially exposed to they would receive the disease? |
|
| 47:35 | It's a measure of contagiousness really. And so a single person that has |
|
| 47:41 | could could spread it to 12 or other people. Okay. Compared to |
|
| 47:46 | like mumps, which is 4-7. it's kind of a measure of contagious |
|
| 47:50 | diseases. Okay. And so then threshold value relates to herd immunity. |
|
| 47:58 | . So you've heard about herd immunity the last two years. Okay. |
|
| 48:04 | basically herd immunity means you have the , the majority of the population |
|
| 48:14 | What that value, it has to . Okay is what the threshold is |
|
| 48:19 | about. Okay, terms of the that needs to be fully vaccinated to |
|
| 48:24 | the herd effect. So what the effect herd effect is is that you |
|
| 48:30 | if you just do it like this I'm here. Okay. All |
|
| 48:37 | And I am sick. Okay. I have um and this person over |
|
| 48:47 | is sick. Okay. And so I say triangle equals fully. Give |
|
| 48:57 | nice person. Okay? So if have the majority of the population is |
|
| 49:11 | vaccinated against that particular infectious disease means the greater proportion of population is fully |
|
| 49:22 | . They can deal with it. ? So basically all the triangles are |
|
| 49:26 | as sinks to absorb the pathogen. ? So the chances of me getting |
|
| 49:31 | from this person. Okay. Is less obviously because I have layers of |
|
| 49:41 | around me that are vaccinated that can it and deal with it. |
|
| 49:45 | Because you're never going to have 100% immunization of anything. Right? Because |
|
| 49:53 | just can't get vaccinated for medical reasons or for for religious reasons or for |
|
| 50:00 | reason. Right? You're not gonna 100% compliance. So this is a |
|
| 50:04 | to protect those people. Okay. , um, so are we in |
|
| 50:11 | state of texas know in the United , are we at her community? |
|
| 50:17 | says yes. Is the United States herd herd immunity levels for covid? |
|
| 50:29 | . We've been getting there for like year and a half. We haven't |
|
| 50:33 | there. We had a In the 30 days or so. Once the |
|
| 50:40 | was out there was we got to about 25-30 In about a month or |
|
| 50:46 | months And it's been since then we've gotten to 66% since then. So |
|
| 50:55 | been it's been like this and then like that. Okay, So we |
|
| 51:00 | not close to her community for inspiring to go back to these values |
|
| 51:05 | So for of course it it will 68% 66% as of yesterday. Countrywide |
|
| 51:13 | terms of fully vaccinated, shot it boosted. Okay. Um That okay |
|
| 51:24 | is like around this this this range the low end. Okay. And |
|
| 51:30 | even even on low end you still to have within three quarters at least |
|
| 51:34 | the population uh for the vaccine now regional differences of course among the |
|
| 51:42 | what's the most? I didn't look all the United States but the what's |
|
| 51:47 | most fully vaccinated ST of? No vaccinated bad. Put your backs against |
|
| 52:02 | which which states in the United highest vaccination, fully vaccinated. Uh |
|
| 52:12 | . New York was 77% I think was up there as well. Uh |
|
| 52:18 | was Georgia at 54 Texas was at or below 54. Well above. |
|
| 52:25 | just had no historical 50 61 or . So anyway. Um But thankfully |
|
| 52:32 | variant that's out there, most common is one that's probably the most benign |
|
| 52:37 | . We're gonna get cold and get now. Um Anyway I've got it |
|
| 52:43 | I've had I've been vaccinated, I've boosted and I've got the and I |
|
| 52:47 | covid. So I think I'm Um So anyway, um Okay. |
|
| 52:55 | look at vaccines. Alright, so , the tables are more just kind |
|
| 53:00 | a summary thing. Don't you don't to memorize, you know, all |
|
| 53:04 | different types of agents that are literally and what types don't worry about |
|
| 53:10 | Um But you know, it's one to note is that there are lots |
|
| 53:13 | them fit into this category of live vaccine. So we're talking about attenuation |
|
| 53:20 | way back from the first lecture to the context of this historical and development |
|
| 53:28 | vaccines and pasture and etcetera. Um uh close as you can get to |
|
| 53:36 | actual live infectious agent actually the better is in terms of immune response. |
|
| 53:43 | the live attenuated vaccines are good are probably the best because it's it's it's |
|
| 53:51 | the most close closest version you have the infectious agent and its ability to |
|
| 53:56 | really key. So because there's differences vaccine types in terms of what are |
|
| 54:05 | are they stimulating the entire adaptive immune . So when you see this differentiation |
|
| 54:11 | it's activating both B cells and several T cells and everything right? Rather |
|
| 54:19 | just relying on activating humor community. ? So live attenuated vaccines, does |
|
| 54:26 | ? All right. They can activate all parts of the that immune system |
|
| 54:32 | means for a better longer lasting Okay. One that relies mostly on |
|
| 54:38 | immunity uh may not be as long . Okay, and ken wayne. |
|
| 54:42 | that tends to be kind of what's with Covid vaccine. Hence it's getting |
|
| 54:47 | . Okay. So but you some of it, I guess it |
|
| 54:51 | to do with the nature of the as well. Right? You can |
|
| 54:54 | can you can only work as well terms of your response as to what |
|
| 54:58 | trying to get a vaccine for. Anyway, so we went to the |
|
| 55:04 | of somebody. So the other thing point out is of course, that |
|
| 55:07 | at toxoid. Alright, so we think about microbes microbes microbes in terms |
|
| 55:13 | infectious disease. But remember that microbes toxic. The toxin itself can produce |
|
| 55:19 | isn't it can be an an urgent can produce antibodies tour the toxins. |
|
| 55:23 | , tetanus shot is basically a It's antibodies in there that will bind |
|
| 55:29 | the tetanus toxin. Okay. It's really about binding to the tetanus producing |
|
| 55:36 | . It's about getting because the effect coming from the toxins that it |
|
| 55:40 | So getting rid of. That is key and and diptheria as well as |
|
| 55:44 | number of microbes that produce toxins that have vaccines for toxoid as they call |
|
| 55:50 | . Okay, so live Attenuated How do you make them uh |
|
| 55:56 | Remember means to limit them or to uh but you do so but the |
|
| 56:03 | the the agents still retains its ability replicate to infect and replicate but it's |
|
| 56:09 | not able to cause disease. So disable the and the balance factors that |
|
| 56:16 | to cause disease. Okay. And um so it's a weekend of |
|
| 56:22 | But of course has all these antigens produces a response it can by by |
|
| 56:29 | virulent genes. You enable it to replicate but not but not to cause |
|
| 56:36 | of course. And so that will all portions of the different response by |
|
| 56:43 | yourselves but not causing disease. Then cells can present an engine And connective |
|
| 56:50 | side of toxic t cells. Um course B cells are activated. So |
|
| 56:55 | mean it actually it's both sides of adaptive immune response which is which is |
|
| 57:00 | good thing. And it's not surprisingly that that's many of your vaccines are |
|
| 57:06 | that type. Okay, measles, etcetera. Um inactivated killed vaccines. |
|
| 57:13 | there is a chance, although I not seen then it's that it's like |
|
| 57:20 | common effect. There's a rare occurrence there is the potential is there that |
|
| 57:25 | can mutate into a form that may infectious. Okay. Although lots of |
|
| 57:30 | testing is done but you can never 100% sure. But they've been using |
|
| 57:34 | back. I forget what they are . The measles and mumps and whatever |
|
| 57:38 | for decades. So but um but if you wanna go a step |
|
| 57:43 | you can with um inactivated killed vaccines these are the variety different ways. |
|
| 57:49 | can do it. Okay uh chemicals course certainly radiation etcetera. Any kind |
|
| 57:55 | stress that kills a an agent is it would do it. But it's |
|
| 58:01 | something that can replicate in your Okay. So you lose kind of |
|
| 58:07 | ability to stimulate as well your your mediated immunity. Okay so like psycho |
|
| 58:14 | t cells et cetera won't be So it's mostly just human community and |
|
| 58:20 | production typically may not last as long it may require repeated booster doses. |
|
| 58:27 | um but again both of these uh and killed. Attenuated, live attenuated |
|
| 58:34 | killed are both dealing with the whole of the whole intact microbe. And |
|
| 58:41 | we're looking at viruses but they can be bacterial as well. Okay. |
|
| 58:46 | the point is to hold the whole being used in both these not the |
|
| 58:51 | in subunit vaccines. Okay so these basically taking parts of the agent and |
|
| 58:59 | the parts of course are antigenics they're immune response. Taking those parts and |
|
| 59:05 | becomes your vaccine. So the different of that. You can simply just |
|
| 59:09 | the purified subject which is going to typically a protein that is your |
|
| 59:15 | Right? That's that's possible. Okay can then take it a different way |
|
| 59:21 | you can just prominent D. A. Gene cloning techniques to just |
|
| 59:29 | the gene that produces that particular engine clone that you can use a bacterial |
|
| 59:34 | to express it for you. Okay then you can isolate the protein that |
|
| 59:39 | . Okay um this method in the of vaccinations really just growing up the |
|
| 59:44 | and just blowing it up and just all the parts and that's your |
|
| 59:48 | Here's here's a more maybe a specific of doing it which I'm just expressing |
|
| 59:54 | engine itself and then isolating it and becomes the vaccine. Um You can |
|
| 60:01 | a vector you can use for example a plasma can be constructed that can |
|
| 60:09 | your agent that you inject. These what we call the DNA vaccines. |
|
| 60:14 | vaccine. And Covid vaccine is not the transcript uses M. R. |
|
| 60:18 | . A. As the uh as vaccine. And so the expression of |
|
| 60:23 | is what occurs. We'll talk about a little bit the competent vector |
|
| 60:28 | So these are basically using the in example the virus shell if you will |
|
| 60:37 | it and then manipulating the of course associated an envelope and associated you know |
|
| 60:44 | and whatnot on the surface as a . And then you put in you |
|
| 60:48 | the genome for what you want to in their different various genes for angie |
|
| 60:53 | things. But then the uh but uh becoming a vector vaccine is one |
|
| 60:58 | can infect a cell and express that . Okay the J. And |
|
| 61:06 | vaccine is of that type. So is the J. And J. |
|
| 61:09 | of this type. And the the modern modern fighter is of that type |
|
| 61:16 | . It's A. M. RNA DNA. Um the virus like |
|
| 61:21 | So these think of these as synthetic maybe. So let's say you can |
|
| 61:27 | a viral proteins and they can kind self assemble into a virus like particle |
|
| 61:34 | you can kind of insert genome of in there and manipulate it. HPV |
|
| 61:41 | , papillomavirus HPV can cause cervical And so this vaccine is constructed that |
|
| 61:49 | at least one of the forms is and so again that's not something that |
|
| 61:55 | is not something that will replicate. . But it can of course be |
|
| 62:01 | as a vehicle to maybe infect the but it's not really going to replicate |
|
| 62:06 | um and so are toxic. We about toxoid is inactivated toxins. And |
|
| 62:12 | um let's look at the place accurate . So as mentioned um your uh |
|
| 62:23 | are your best engines in terms of a very strong immune response followed by |
|
| 62:29 | and then a little bit lower down . Okay, so place cycle rides |
|
| 62:35 | of course never pathogens have have a . These are of course carbohydrate in |
|
| 62:41 | . And so but they tend not be uh as good in terms of |
|
| 62:46 | immune response but they do produce some not but not as good as it |
|
| 62:50 | be. But you you use what would use what you can write. |
|
| 62:55 | for example meningococcal vaccine that I'm assuming all got before coming to school. |
|
| 63:02 | Meningococcus is um it's very thick And so there's like five different engine |
|
| 63:07 | I think that we used as is streptococcus pneumonia i which is the pneumococcal |
|
| 63:14 | . So that one the meningococcal is for younger people. Uh The most |
|
| 63:19 | one is given to those my age older on the other end of the |
|
| 63:23 | . Okay. But not necessarily a . So you tend to be only |
|
| 63:27 | uh promote the humor immune response. but you can bring it up a |
|
| 63:36 | by adding a protein to it will a conjugated vaccine. Okay, so |
|
| 63:42 | can put the addition of a protein there to boost it up somewhat. |
|
| 63:48 | . And uh and so adding a enables a T. Cell activation to |
|
| 63:57 | as well. And so if you we talked earlier about The Place |
|
| 64:02 | Big Place Ackroyd can initiate activation of cells that um the T independent |
|
| 64:10 | Right? And that only produces plasma . Okay. Uh that produce antibodies |
|
| 64:16 | you're involved with T cell now t . Now you're not refuse plans myself |
|
| 64:21 | also a member itself. And that's definitely a good thing. Okay so |
|
| 64:26 | can help. And the example he here uh yeah there's a number of |
|
| 64:32 | to actually do this where they had had a protein to it to help |
|
| 64:36 | out in terms of immunogenicity. Um so okay gasses vaccine. So |
|
| 64:42 | you see um a uh here's a . Okay, so here's the |
|
| 64:49 | We would take out the uh isolate gene for the engine that produces a |
|
| 64:56 | and then insert that into a vector would be a plasmid vector. And |
|
| 65:02 | this is your product, this is bank scene. And so this to |
|
| 65:07 | what's called the gene gun sounds kind dramatic but it basically contains a solution |
|
| 65:12 | the plasma injected. This is going be an intra muscular injection. And |
|
| 65:19 | muscle cells are multi nuclear state. um plans with interest and absorbed by |
|
| 65:26 | cells that can express the gene prison . And then this can elicit a |
|
| 65:35 | by both T cells and B So it can give a very good |
|
| 65:42 | . Um the the covid vaccine is finds her is similar to this |
|
| 65:49 | correct becoming a vector vaccines. Um using a virus vector. So |
|
| 65:55 | a DNA virus um that's when that's used heavily for a number of years |
|
| 66:02 | in this capacity as a vehicle to put in a in this case is |
|
| 66:08 | flu flu vaccine. So the influenza gene or genes are then cloned into |
|
| 66:16 | I don't know virus genome Of course coronavirus the jeans and the hantavirus genome |
|
| 66:21 | inactivated That would enable it to cause . So uh so this but this |
|
| 66:27 | can infect the cell and uh that will express these antigens again, showing |
|
| 66:34 | to the immune system. Okay, and J vaccine is like this. |
|
| 66:40 | , so if we look at covid then we have a pretty familiar with |
|
| 66:46 | illustration. Uh remember the spikes out are the tell me are of |
|
| 66:52 | That's what the vaccine the engine is the vaccine that uh in its |
|
| 66:58 | Okay. The yellow ones here, proteins and for the Moderna Moderna Advisor |
|
| 67:06 | , something like this. Okay, usually M RNA. Okay. And |
|
| 67:14 | from the covid virus despite protein, gene for that's what we want to |
|
| 67:19 | . And so we get this out the way. So the so the |
|
| 67:27 | , the there we go. So if you recall uh looked at bacterial |
|
| 67:35 | and compared them to eukaryotic jeans, you can have a lot of processing |
|
| 67:40 | goes on, right? We'll form transcript and then the transcript has to |
|
| 67:43 | stuff put on it and then we to chop it up right to make |
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| 67:47 | translatable transcript. So that's what you here are these elements to cap and |
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| 67:51 | tail. You tr these are all a an army transcript must have if |
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| 67:59 | going to be translatable, right? have these elements. It's not going |
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| 68:05 | work. Okay, so of course genie in the middle is this gene |
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| 68:10 | the spike collectible protein here. Okay um so these were constructed and then |
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| 68:18 | is what basically comprises the vaccine. it was a bit simplistic because it's |
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| 68:24 | just um just having M. N. A. Suspended in the |
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| 68:31 | is not gonna work very well. don't think because RNA s aren't by |
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| 68:37 | aren't inherently super stable. Okay they break down so you want to have |
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| 68:44 | delivery system that will keep that will them basically. But we'll look at |
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| 68:53 | here in a second. But the of the MRT of course to sell |
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| 68:58 | enable it to then express it and the engine is expressed on the |
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| 69:02 | And then of course that can involve cells B cells produce antibodies uh these |
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| 69:08 | what we call neutralizing antibodies that will the virus and then severely hindering its |
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| 69:16 | to infect cells obviously. Okay so is the actual process. Um again |
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| 69:23 | don't need to memorize the slides but is the the colonial of the |
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| 69:28 | Expressing it in terms of the Um but then again like I said |
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| 69:34 | don't just suspend these RNA is in liquid and off you go have a |
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| 69:39 | . They use this vehicle here called lipid nanoparticle which is something it's not |
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| 69:44 | lipid bi layer right? That you 22 layers of lipids here but it's |
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| 69:49 | bicycle. It's basically coding something as shell to hold these um transcripts |
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| 69:57 | And so uh this is a delivery that's going to have it's gonna be |
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| 70:02 | to maintain the viability of these transcripts better than if they're just not enclosed |
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| 70:08 | that. Okay. And it is course is something that will that can |
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| 70:14 | with a a membrane and then enable into the cell. Okay, so |
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| 70:23 | the now the J and J Okay, so this this is not |
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| 70:30 | a a pre existing microbe or right? It's just they artificially constructed |
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| 70:38 | membrane around it, if you Okay, proprietary technology. Of course |
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| 70:43 | did this company developed um and of tested out the wazoo I'm sure uh |
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| 70:48 | to work optimally. Um now the and J vaccine. Okay, so |
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| 70:56 | little different strategy using remember the predominant vector model. And um the spike |
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| 71:06 | for the spike protein of course is closing to the vector which is then |
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| 71:12 | the virus here. Um then the oops, sorry then we in fact |
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| 71:23 | vaccine contains these viral particles with the containing the gene for the spike protein |
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| 71:30 | effects the virus infects so and so . So basically four steps 4 and |
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| 71:38 | , what's different, of course with and J is the delivery system. |
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| 71:41 | . And of course we're expressing uh to the energon and and showing the |
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| 71:46 | . That's the same as with the Advisor vaccine. So this process is |
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| 71:50 | same. They're just a construction. the front part of the strategy is |
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| 71:55 | little different. Okay, so, , again, producing the same type |
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| 72:01 | neutralizing antibodies. Ok, so, , stop. Okay. Hey, |
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| 72:08 | questions? Yeah. Pretty much. than you have, um, It's |
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| 72:19 | just the transcript itself, it's part the gene is part of a chromosome |
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| 72:23 | or a larger vector than than than Pfiser one. Right. Right. |
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| 72:30 | . Thanks folks. See you |
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