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00:02 | You say you? All right we'll get it started despite the block |
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00:47 | the middle of the screen. that's where we're at underneath that |
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00:52 | Ok. So we are gonna be here in a couple of minutes. |
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00:57 | . So, um, so, , we have a quiz tomorrow, |
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01:07 | quiz. Um, and I answer you on Monday, uh, today |
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01:13 | gonna finish up 17 and the next starting to, uh, 15, |
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01:21 | last part of this. Ok. , the last part of this. |
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01:29 | . Um, uh, microbial Ok. So we'll have plenty of |
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01:34 | to finish that up next week and , uh, uh, then it |
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01:38 | next unit, the last unit week and then they, uh, |
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01:41 | there is still a ways away. , uh, you know, two |
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01:45 | . So remember that the schedule opens , I guess, uh, technically |
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01:50 | midnight. So this morning. uh, if you need to get |
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01:56 | slot, uh, or slot then guess you could be up at |
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02:01 | Ok. Um, let's see. , oh, it's just not |
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02:07 | Ok. Still going. So, , anyway, we'll stop. So |
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02:10 | gonna start with, um, third question. OK. You may |
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02:14 | . If you've gone through the you may know it may not. |
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02:17 | OK. We'll work around it. , but let's look at this |
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02:22 | It almost placed it right. Let try again. Come on. All |
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02:28 | , let's try this. OK. gonna do like that now. T |
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02:37 | on. Uh Yeah. OK. ? Uh I don't know what the |
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02:49 | this is. OK. Um All . Let me, all right while |
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02:56 | answering the question. Let's see. , thank goodness. OK. All |
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03:02 | . So going to weird spacing that how I could get around the block |
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03:06 | . So secondary immune system response. that do a memory B cells |
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03:13 | Is that what they do or can do that? A Glutin Nation Company |
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03:18 | Cells by antibody that true or false Cytotoxic T cells. Is that what |
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03:25 | do? OK. So we will all this today. OK. So |
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03:31 | get through these. If you're not what they are, we will hopefully |
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03:34 | by the end today. Um Let's see. I'm sorry, I |
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03:42 | to open the pool. So if answer, try it again. Um |
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03:49 | . But there uh so um we're on this so kind of a uh |
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03:57 | a little bit. We started this uh at the end of last |
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04:02 | So um the that of new So remember that's the third line of |
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04:07 | , right? Um Your innate immune , physical chemical barriers. Um Different |
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04:14 | types involve um processes involve fever, et cetera. So, um non-specific |
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04:24 | they call it uh Here is more because it involves binding between molecules specific |
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04:31 | between molecules. And so that's what about uh the effects of the adaptive |
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04:37 | system. So that's what we'll discuss . And the false answer here is |
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04:51 | yeah. Uh A gluten a clumping , that. No, that's |
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04:57 | Sorry go. OK. The false is um so A is true. |
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05:04 | . Memory B cells. Um That's uh are built up. That's part |
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05:09 | the vaccination. Uh Outcome is ultimately lots of memory B cells um |
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05:16 | they can bind to both antigen and cells at the same time. |
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05:21 | We'll see that very quickly here. A rotation is clumping of cells by |
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05:27 | . OK. So toxic T cells with intracellular pathogens, not electric cell |
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05:34 | , that's the fault state. Um So cytotoxic T cells interact with |
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05:41 | cells. So virus infected cells, example, can be detected by cic |
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05:47 | cells and gotten rid of, So the B the B cells would |
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05:52 | with extra cellular pathogens through antibodies. . So let's uh so we'll cover |
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05:58 | these here today. Uh So we went through kind of an overview |
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06:04 | the whole process here that immune The key thing is and that's what |
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06:10 | response to. OK. So it's a, there's a recognition component. |
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06:16 | de a detection component, a recognition and then uh a recognition and binding |
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06:25 | then that brings about various effects. . So we went through uh so |
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06:30 | these two halves here can be uh can associate basic two basic functions. |
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06:36 | is the humoral immune system. The cells uh respond to extra C of |
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06:42 | . OK. So antibodies do their outside of cells. They can't go |
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06:46 | of a cell and buy an an . They have, they're external intercellular |
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06:52 | are dealt with by cyto topic T . Uh T helper cells have a |
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06:58 | of different roles and we'll see how develops today. Uh One of |
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07:02 | one of them is to interact with cells to activate them. OK. |
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07:07 | is to interact with macrophages and dendritic . OK. And um these uh |
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07:21 | part of the remote, we call things. Um for short A |
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07:28 | which means antigen presenting set. So are cell types that can, that |
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07:33 | both be part of the innate immune and baby supplies. Uh but also |
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07:38 | of the interact with the adaptive immune and work with certain T helper |
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07:42 | OK. So there are unique cell in that way. So that uh |
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07:48 | can work on both sides. Um uh cell we'll go through these. |
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07:54 | so the other thing to remember is uh antigen epitope, right? |
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08:00 | antigens are on the surface of a . OK. And um they will |
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08:07 | , they can be a number of um molecules, typically, proteins, |
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08:12 | can be like proteins, carbohydrates, cetera um that are on the periphery |
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08:18 | it can be, it can even a Flagel. Ok, a cell |
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08:21 | , a capsule, uh outer membrane a ram negative, et cetera, |
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08:24 | cetera, uh viral proteins on the . So, uh these are the |
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08:29 | antigens interact with antibodies interact with. so we are closer to the finding |
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08:36 | than an antibody. Oh All look that up, there will be |
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08:42 | area within that antigen should engrave red where it actually binds to. So |
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08:49 | call that the epico right. So the, if the square here is |
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08:54 | antigen, right, then this smaller inside is what it's binding to. |
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09:01 | we call that the epitope. Um So uh so as we look |
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09:08 | further at antibody structure, OK. antibodies basically think of it as a |
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09:12 | , right? So letter Y with couple extra things on it. |
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09:16 | So um there is regions that are what they called constant regions. |
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09:24 | Um And variables. So these change antibodies to antibody out here, |
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09:30 | This is the antigen binding sites. ? They're called variable sequence. They |
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09:36 | in amino acid sequence and it depends what they bind to, right. |
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09:40 | your ability to bind all types of and there's like the the number of |
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09:47 | you have that can respond, you theoretically respond to like got into the |
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09:53 | it's a super crazy number. It's a 10 to the 15th or something |
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09:58 | that. Uh Possible types of different that are out there. So remember |
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10:03 | have engines that are part of a like pathogens and viruses and protozoans and |
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10:09 | and whatnot. But I also remember like um different chemicals can be |
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10:15 | be an antigen, uh pollen. , I all aware of that in |
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10:19 | , uh ragweed, et cetera. these kind of things serve as uh |
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10:23 | antigen that can stimulate your immune Sometimes not in a good way if |
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10:28 | got allergies on it. So, but uh the, the in |
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10:34 | you have, so you have five here. IgD and IG stands for |
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10:40 | . OK. So immunoglobins uh GDEM uh A OK. Now, uh |
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10:48 | something you need to know, but for your own knowledge. So you |
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10:53 | identify a G ad A E uh , and a based on similarity in |
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11:02 | constant region. So in other all IG Ds are gonna be the |
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11:07 | in that area. All IG DS the same. So that's what, |
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11:11 | , that's how you can identify each . Uh What does that, what |
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11:15 | that part of the antibody look And so each class will have its |
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11:20 | sequence there. OK? And they , and they all be the |
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11:24 | OK. But of course, they'll out here. OK? Because you |
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11:29 | , you can have thousands of IgG and some respond to this engine, |
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11:36 | respond to that engine. So they're be different in the, in the |
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11:39 | and body parts. OK? Uh so what else? So we |
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11:44 | So as I mentioned in the so these parts or that are variable |
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11:50 | to antigens, of course. But then this part combined with a |
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11:54 | , right? So this can be um a macrophage for example, well |
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12:00 | a macrophage but it can be a it can be a B cell for |
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12:05 | . OK. Um That's how these actually work. They have antibodies in |
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12:10 | surface, they find the hands. . So uh that is true. |
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12:14 | you can have both those but remember it could be I'm just uh brain |
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12:20 | . It could be a macrophage because the optimization process, right? Optimization |
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12:27 | when a macrophage binds this part and these parts are stuck to the pathogen |
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12:32 | take the whole thing, right? the optimization. So yes, uh |
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12:37 | of them be cam as well. the point is and and some antibodies |
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12:40 | do this, they can find the and they can bind the other other |
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12:44 | to itself. That's what we call FC portion, right? So an |
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12:49 | portion, a cell can have a FC receptor to it right now. |
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12:57 | Let's see. OK. So it's a couple of questions that relate to |
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13:02 | function. So we're gonna go through five different classes and then um uh |
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13:10 | of see what their functions are, get a little more information on |
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13:14 | Uh These, these are located sometimes different body fluids. Um they can |
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13:21 | different functions, of course. Um here it's asking antibodies found on mucosal |
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13:27 | in mucosal secretions and functions to interfere pathogen adherence. OK. So this |
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13:35 | part of that. Um you could this part of the chemical barrier, |
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13:40 | . So remember that your physical skin uh mucus membranes, they have |
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13:46 | secrete some kind of fluid and the will contain different types of antimicrobials, |
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13:52 | ? It can be something lysozyme uh this particular antibody can be in there |
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13:58 | well, right? So let's speed this up a little bit. |
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14:06 | what can happen? 10. Let me see. OK. |
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14:21 | All right. Yeah, it's gonna IG A. So IG A is |
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14:27 | uh one of the big um major ways of pathogens are able to stay |
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14:34 | your body is they adhere to your membranes. So that's kind of where |
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14:39 | live in many cases. So um meningitis organism, uh lots of respiratory |
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14:46 | uh that enter through your nose or throat, uh need to have mucosal |
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14:51 | . And oftentimes they have ways to they need to stick to your, |
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14:56 | these uh membranes and if there's an A, it can bind to it |
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15:00 | then block its ability to stick that a good uh defense for those types |
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15:06 | pathogens. Um OK. The Hallin . OK. Is the specialty of |
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15:16 | Pyramid. Pera Pitta me, excuse . Um I mean, like, |
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15:22 | we'll learn that um industry is the choices and as are shown the uh |
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15:31 | antibodies can um just be in the form, the singular Y form. |
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15:39 | But some can group together like this not always in groups of five, |
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15:45 | in groups of two. So IG can actually do that. OK. |
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15:51 | um uh and that kind of it , it enhances their funk, |
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15:57 | So it used to have, they two sites, right? We're just |
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16:02 | this form, you'll have two engine sites. 12. But if you |
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16:11 | , all right, now you can 41234. So it kind of increases |
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16:19 | ability to bind, to bring, bind up uh energy. OK. |
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16:25 | uh even more. Oops, even uh timer. All right. |
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16:39 | right. This thing closed prematurely. fault. Let's try it one more |
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16:43 | . Sorry. This is um there go. So yeah, it's gonna |
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16:50 | the function of those types of not all of them do it, |
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16:54 | some can form these multiple groups OK? Um All right. Counting |
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17:15 | . So one, all right, we go. So uh it |
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17:23 | I believe that's m correct. So is forms these uh types of |
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17:30 | And so what happens is they can up a bunch of cells at one |
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17:35 | um having basically 10 and your binding . Um And so the last one |
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17:43 | is about this function of, of so that can uh certain antibody types |
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17:55 | their function when sitting on top of cell, right? Others can be |
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17:59 | floating, OK? Igaigm. Um others only work, I just gave |
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18:07 | a hint there others only work and sitting on top of the cell and |
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18:12 | how they function. OK? We down to nine. All right. |
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18:28 | this is going to be um IgD IgE. So it's actually uh C |
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18:37 | D. OK? So both of work I sit and talk about uh |
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18:45 | yeah, all time. OK? we'll talk about that now. So |
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18:49 | I just mentioned earlier the IG right? So again, there in |
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18:54 | percentages you don't need to simply memorize percentages. But uh ID A is |
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19:03 | is not need and percentages that they're in blood. OK. So it's |
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19:07 | because it's mostly found in the culture , right? Uh your nose, |
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19:12 | throat, you know, body cavities aligned with the mucosal membrane, |
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19:18 | And so what they do is what's a neutralizing function. So, neutralizing |
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19:25 | uh by binding to the microbe, ? They can effectively prevent it from |
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19:31 | cells and binding to your cells. . That's what neutralizing antibodies do. |
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19:37 | . That's what uh COVID vaccine promotes antibodies. So, by coding the |
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19:43 | , the virus can't stick to your or your respiratory tract. OK. |
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19:49 | And so IgG is typically what they the workhorse antibody. It can, |
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19:57 | uh it typically shows up, it's the main, main one in |
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20:03 | to a, a pathogen or in vaccine. Uh versus IgM and IgG |
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20:09 | large numbers. OK. And they a number of functions to um be |
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20:16 | Selman. So help with oc cytosis activate complement uh the neutralization of |
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20:22 | They have a lot of these functions uh that are important in fighting |
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20:26 | OK. Um So they're gonna be , at the highest concentration in the |
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20:31 | . OK. The uh IgD is of those that works by sitting on |
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20:36 | of a cell. So they would on B cells and B cells uh |
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20:42 | the ones that produce antibodies. So hands and binds to these antibodies on |
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20:49 | surface that will stimulate the B cell produce more antibodies. OK. |
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20:55 | um B cells typically have IgD A have IgM on their surfaces. |
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21:02 | And that's how the engine binding leads them, doing their functions. |
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21:09 | Um And so because B cells are found in lymphatic fluid and lymph tissue |
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21:18 | outside the blood, you don't see at very high concentrations in the |
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21:23 | they're sitting on the B cells which not in the blood out in the |
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21:27 | system. Ok. Um IgM, the one that forms the P |
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21:33 | So it will form. So, is clumping. Autin is the clump |
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21:39 | together. OK. And so um what it can do by by doing |
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21:45 | agglutination function, it reduces the numbers infectious units, the body has to |
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21:52 | with. So it kind of concentrates . So if we have, for |
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21:55 | , 10 pathogens, uh when this forms these um P forms, |
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22:03 | Uh with 10 binding sites, it can clump up a number of |
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22:09 | microbes uh at the same time. now you've reduced 10 infectious units on |
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22:14 | left down to one that the body to deal with. So it's an |
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22:18 | function in terms of uh concentrating and dealing with these, dealing with an |
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22:23 | agent like this. OK. And lastly, IgE, right. So |
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22:28 | , they're found low amounts because basic are typically uh not in high concentrations |
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22:34 | the blood right there in the surrounding . And so uh those that have |
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22:40 | allergies or hypersensitivities or hay fever, like that. You can blame this |
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22:46 | here, mass cells or basal pills IgE on top that binds the engine |
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22:52 | sometimes it works too well. You a hyper response and that's what causes |
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22:57 | of, of, you know, eyes and these kind of things. |
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23:01 | . An inflammatory response can result. . So uh but so bays mass |
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23:07 | , there are things kind of to various types of chemicals, like I |
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23:11 | , in response to inflammation and, these kind of things. Ok. |
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23:17 | ok, so those are the five . And so um so your |
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23:22 | and again, so remember that these are released that collect the term |
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23:26 | right? For these things work on immune system cells. OK. Um |
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23:33 | right. Any questions at that My hand hand about the structure |
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23:38 | OK. Uh So let's look at question. OK. So this |
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23:46 | so now we're gonna get into more cell function from T cell function. |
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23:52 | . So uh B cells, most human immunity, T cells mediate certain |
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23:59 | . B cells can differentiate into antibody plasma cells. A single coronal population |
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24:07 | plasma cells can produce antibodies to many ops. OK. T cells can |
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24:13 | kill infected host cells but these cells cannot directly kill cells. OK. |
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24:31 | . OK. That OK. Let's see. Koo. OK. |
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24:56 | the sides to me, right? So um let's just go to the |
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25:09 | up. So T cells can directly infected host cells. Um The B |
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25:16 | themselves cannot directly kill cells. That's . OK. So T cells like |
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25:21 | cytotoxic T cell um can kill an cell. These cells themselves don't kill |
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25:27 | but they can, they, their is through antibodies on their surface, |
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25:32 | ? They don't actually kill anything but antibodies they produce can lead to different |
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25:37 | . Ok. So this is Um The single of population of plasma |
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25:46 | can produce ops to many different or produce antibodies to many different ops. |
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25:51 | Is that true? Yeah. Image uh BTS. Anybody is false. |
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26:00 | think it's hot? Don't be afraid name is false. My name is |
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26:10 | . Yes. Why? Oh Come on. Why? I know |
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26:16 | Jesus tells me what's the operative words ? What is a, a colonial |
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26:28 | is? What? They're all if you have a clone, you're |
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26:35 | what the same, you're identical. . Um They're the same. So |
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26:44 | single clonal population of plasma cells produce . Too many different ops. So |
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26:49 | they, if they're all the are they gonna produce different antibodies? |
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26:56 | clones, they're gonna produce the produce , that same. Yes. Say |
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27:04 | be confident goodness, the same So that's what a clone, a |
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27:10 | population is. They make, they the same function, same thing. |
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27:16 | A and so a clonal population will antibodies to only one epitope. That's |
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27:21 | basis for your antibody response to vaccine for, for an infection. |
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27:29 | So that's the false one. Um cells can differentiate into antibody supreme pasmo |
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27:36 | of, of course, that's And that's true. OK. So |
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27:43 | all right. So let's see how happens here. OK. Question. |
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27:51 | , I got batteries. Hold All right. Well, that's doing |
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27:54 | . Let me turn this on. . So, um, with humoral |
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28:04 | immunity, we're talking about B cells their function. Ok. So, |
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28:19 | , remember though they deal with extra pathogens? Ok. So, let's |
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28:38 | . All right. Uh So um, so there's two pathways, |
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28:44 | one that's most common is what you're see here on the screen. That's |
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28:49 | um uh the T cell T cell and dependent process. OK. |
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28:57 | in other words, it requires the cell requires a T cell to be |
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29:01 | of the process. OK. The part we'll talk about next is |
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29:06 | The B cell that does not require T cell to activate it. |
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29:10 | So um so what happens is androgen an by an by will be on |
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29:17 | of the B cell. It can a uh IgD and IgM sitting on |
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29:23 | and binding an antigen to. It occurs as well as B cells will |
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29:30 | these antic fractions. OK. And um so I remember B cells are |
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29:37 | cells, dendritic cells and um uh have these uh uh class two types |
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29:47 | MH C molecules. OK. And they'll show antigen. So B cells |
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29:52 | be antigen presenting cells. OK. so they use that function to interact |
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30:00 | the T cell. OK. So that antigens, T helper type two |
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30:07 | respond. OK? And they in activate it into a antibody producing plasma |
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30:16 | through the act in the B turn it into a plasma cell as |
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30:22 | as into memory B cells, So both are the result of this |
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30:27 | . OK. So again, this what's called the T dependent antigens, |
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30:32 | ? And these tend to be the common ways to activate a B |
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30:36 | OK? To involve TT helper cell it. OK. And so, |
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30:43 | so the uh so the uh other that happens and uh let's see this |
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30:53 | next. It's in a couple of , but there's a process why a |
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30:57 | independent type doesn't need to help with T cell. And we'll see that |
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31:01 | . But let's look first at this clonal selection process. So, what |
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31:05 | talking about is when an engine is , OK? You're gonna have pools |
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31:12 | B cells, right? Thousands of of B cells, right? And |
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31:17 | each will have antibodies sitting on top each pool will be able to theoretically |
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31:23 | to any energy that's out there. . So that's what this is about |
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31:28 | . This is what clonal selection is you're gonna have. So here just |
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31:31 | it simple. 1234 populations of right? Each one, each one |
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31:38 | itself is a, is a, the same, OK? Is a |
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31:45 | population. So this is one, all have the same anti body that |
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31:49 | to the same antigen, right? is one that has binds to a |
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31:54 | engine. All bind to that same so and so forth. So we |
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31:57 | four groups, you know, your will have thousands of these. |
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32:01 | So um so as an engine comes here is red, so red, |
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32:07 | . Uh presumably it will bind to antibodies of one of these populations. |
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32:13 | ? This this example, it's binding not 123, but number four, |
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32:18 | . So any B cells that that are four in the four |
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32:22 | four C group, OK will bind antigen. OK. And then only |
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32:29 | group then goes on to differentiate. . So they will produce well what's |
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32:36 | clonal expansion. So you have a cells here that then correspond to angel |
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32:41 | divide. OK. So you produce population of clones. OK? And |
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32:49 | they differentiate into memory b cells and cells. So plasma cells are the |
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32:55 | ones that may OK. Uh The of a plasma cell is about 60 |
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33:03 | . OK. Then they die, ? The plat the memory cells of |
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33:07 | can last for decades, right? can last 3040 years. OK. |
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33:14 | sitting in your body waiting for the time that the engine reappears, then |
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33:19 | can uh start the producing antibody. what happens is when the when the |
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33:25 | cell get stimulated, then it differentiates a plasma cell and more memory |
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33:32 | OK? And it's the plasma cells won't produce the through the antibody |
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33:38 | So, uh but you know, cells, although they can last a |
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33:43 | time, um some do kind of their what's called immunogenicity over time. |
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33:51 | they're not as strong in terms of to an engine as they once |
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33:55 | right? So that's kind of figures why you need a booster shot every |
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34:00 | and then for certain like tetanus, example, you get a booster shot |
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34:03 | every 10 years or so as well certain other other uh vaccines. So |
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34:09 | is kind of meant to boost up population of memory cells. OK? |
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34:14 | But the um the uh T independent , OK? They don't require this |
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34:24 | via BEA OK? And so the is so I'll jump back to this |
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34:30 | this next thing I'm gonna show you only for explanatory purposes are not gonna |
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34:36 | tested on OK? But it, , it's the only way to kind |
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34:39 | tell you how you differentiate these two . OK? The T dependent engine |
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34:45 | itself requires um energy, of binding to the body of the |
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34:51 | So here's a s what you would a small engine, right? Compared |
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34:56 | a big super big molecule, like a big sugar polymer or |
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35:01 | right? So this is like this called an average sized antigen. |
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35:05 | Typical, typical size, right? what has to happen is because you |
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35:11 | , antibodies can have two binding they interact right in the bond antigen |
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35:16 | they form what's called a B cell . And so this process of binding |
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35:21 | kind of coming together, it's called . Again, don't worry about |
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35:26 | I'm just kind of show you how happens. Uh This then leads to |
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35:32 | MH C molecules showing it also comes the cell and it shows it |
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35:38 | And so this process only happens with dependent uh in the T dependent |
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35:44 | But uh with your more typical size , it's the more common way. |
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35:50 | ? Now another way to kind of those antibodies together, OK, bunches |
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35:55 | them together to act to activate the is to do this, I could |
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36:02 | that. You see this big long , right? So we can bin |
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36:08 | bring together a bunch of the antibodies the surface because it's so big. |
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36:13 | that's what accurate the E cell receptor makes the, the cell able to |
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36:17 | produce antibodies without the contribution of a cell getting into it. OK? |
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36:25 | That's really the basic difference. T , this one and T dependent. |
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36:32 | it's about the size of the OK. And um like I |
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36:38 | the more common is with, you , these regular size, I call |
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36:41 | size, uh typical sizes. Uh can, this can happen, of |
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36:46 | , it does. But uh they these really large ones. It's not |
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36:50 | common, but it you know, happens as well. OK. Um |
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36:57 | Yeah, so the other thing to is that once it's uh activation |
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37:02 | which mechanism you are gonna hang path and memory cells form. OK. |
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37:07 | that really is what forms the basis vaccination. OK. Um Let's uh |
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37:17 | about this. So any questions this ? OK. So uh so, |
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37:24 | talking about vaccinations, this could this could be vaccination, it could |
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37:28 | initial exposure due to va v OK. And so the uh uh |
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37:37 | . So again, this is AAA that occurs over uh several days because |
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37:46 | um your body has to recognize detect it. Number one, recognize |
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37:52 | and buy into it. And that's a time on to that. |
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37:55 | And so uh there's always gonna be time to evolve for that reason. |
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38:00 | you see there you go to an takes about a week right before we |
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38:05 | to see um a response by the well, detectable response. OK. |
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38:11 | so what happens is initial exposure? is the primary response. OK. |
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38:17 | Andrew is introduced whether through vaccine or and uh first antibodies form are, |
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38:26 | IG MS, right? They form the Pinter forms, right? And |
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38:30 | then followed by IGV, as I before, this, this whole process |
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38:35 | antibody formation and, and um uh immune system in general, the ad |
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38:41 | in the system is very complicated. um because you do, they'll talk |
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38:46 | it here. But uh there's a curve for these cells and the energy |
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38:53 | binding. OK. So initially, IG MS aren't that great. |
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39:00 | Uh But because they have the pension , that helps because you can clump |
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39:04 | a number. So even if you , even if the binding is not |
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39:08 | great, OK. But then the that follow. So, so you |
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39:14 | , you can have a B cell . OK. So, all |
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39:20 | And um so it binds antigen and G is short for antigen. And |
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39:29 | this B cell will first produce Well, plasma cells will OK. |
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39:36 | then these will be kind of not super Bindy to antigens, but they'll |
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39:41 | well enough. But then it's kind a learning curve and part of that's |
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39:44 | of continued binding, helps it bind kind of a thing. OK. |
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39:48 | then these cells then switch to OK. So the same B cell |
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39:55 | responded from IgM can also then switch a different antibody type G type, |
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40:02 | ? So what's called um class Don't worry about it, but just |
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40:07 | of showing the versatility of these, these types of cells. So B |
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40:12 | can first do this and then the one can then do the other |
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40:14 | OK. And in the second the IgG tends to be a better |
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40:20 | . So IgGs are are kind of work course as I said they have |
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40:24 | of different functions. So, and get a big response from them as |
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40:27 | see in the blue line there. of fact. So, so your |
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40:32 | so in your primary response, it a long while because you're just, |
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40:37 | your first exposure and again, your system cells have to find it, |
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40:43 | it and then do their thing that time, right? So, but |
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40:46 | you're doing in that in that right is making uh plasma cells and |
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40:52 | b cells. OK? And memory cells you're putting away storage so you |
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40:58 | call on them later. OK? positive cells will be the ones pranking |
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41:03 | and will live for about a couple months. OK. So if you |
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41:08 | um second exposure, whether it's through uh an infection by the same pathogen |
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41:15 | a booster shot, right? Then response is much quicker. The timeline |
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41:21 | as long, right? More And so uh and that's because you've |
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41:27 | memory cells ready to go, You form those in the primary |
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41:32 | Now they're ready to act and energy long boom. And you're forming plasma |
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41:37 | to make antibody and you form more cells. OK? So that's why |
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41:42 | response is much quicker because they're, primed and ready to go. |
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41:48 | Um And of course, that's obviously nature of white and booster shot is |
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41:51 | really enhance that response and make lots memory cells OK. Um, now |
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42:02 | uh, and some vaccines do this than others and we'll talk about |
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42:06 | We'll talk about vaccines in, in little bit of detail later. But |
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42:12 | vaccines are better at this than others terms of producing lots of good antibodies |
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42:17 | a big response. And there's reasons that. We'll, we'll talk about |
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42:21 | later. Um, any questions about ? All right. Uh Right. |
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42:29 | so what ha what are the what are the end results of the |
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42:33 | body? And an and B? . Well, there's multiple, we've |
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42:36 | a couple for the the hallucination the bindings that reduces numbers of, |
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42:42 | infectious units um to by clumping and , the nature of having two binding |
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42:49 | , right? Even better if you form that, that Pru or like |
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42:53 | the IgM can uh ization. We've about that before, right? Enhancing |
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42:59 | cytosis neutralization we mentioned earlier. Uh know, of course, remember that |
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43:04 | are uh can you can form antibodies toxins or like tetanus. Um And |
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43:10 | if and toxins depend on binding to cell and getting into the cell and |
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43:16 | damage. So if you can prevent , and that's what neutralizing an bodies |
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43:20 | . They cope pathogen or the And now these things can't bind to |
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43:25 | cell and do their damage. Basically, you're neutralizing the pat think |
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43:31 | it that way. OK. Uh compliment, we've talked about that |
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43:35 | So anybody can do that. That's classical pathway. And then um then |
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43:44 | the, this one right here. I think I may miss this earlier |
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43:51 | this is uh A DC C for uh standing for antibody pendant cars |
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43:58 | Uh C mediated brings a number of to the party cytotoxicity grows up thinking |
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44:04 | death of the, in this parasite. These are for ABC C |
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44:11 | for a large parasite. It's like large worm. Uh protozoan, what |
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44:16 | you amoeba? What have you a large? Ok. Not your bacterial |
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44:22 | , your viral size, but my . And so uh so to bring |
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44:27 | down, that's that big is gonna a collective effort, right? Gonna |
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44:33 | lots of cells. And so the to do that is to use antibody |
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44:39 | your mechanism from antibody to the parasite bind the cells combined with the combined |
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44:48 | that FC part of the antibody. so things like Eoin Il can do |
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44:54 | . So from your ails are toxin cells. So you get as much |
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44:58 | these together hand body finding, I collectively they release a toxin, overwhelmed |
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45:07 | can come in as well, releasing chemicals. So uh it's a way |
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45:12 | have cells stick all across this parasite antibodies and then together kill it. |
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45:19 | . Um So all these result in you know, chilling of the microbe |
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45:25 | uh not allowing to attach, which can you can get rid of it |
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45:29 | the system this way, uh killing here, of course, in ox |
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45:33 | clumping it, this can uh this bind up bacteria and uh maybe macrophages |
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45:40 | things can come and involve them So the end result is uh |
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45:44 | to get rid of the passengers, , OK, in different ways. |
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45:49 | , um so again, this thing is these are all all extracellular. |
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45:54 | all these are all extracellular pathogens that being dealt with here, T cell |
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46:00 | where we talk about dealing with infra , right? So uh speaking of |
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46:06 | cells, so here is cytotoxic T . So these uh interact with your |
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46:14 | that may be potentially infected. Uh differentiation between T cell interaction with your |
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46:24 | is through the MH C molecules. ? And so remember macrophages, they |
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46:31 | cells, b cells have MH C , right? And that's what T |
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46:36 | cells interact with. Pic T cells with MH C type one, |
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46:43 | So remember if you're not a B , you're not a micro or you're |
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46:48 | a dendritic cell, you're basically every cell in your body, right? |
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46:52 | cell, liver cell, neuron, cell, bladder cell, whatever, |
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46:58 | ? Your body cells, uh if become infected, then potentially a T |
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47:04 | can find it and kill it. . But they can only do that |
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47:09 | the infected cell showing what's infecting it the body. That's where the Mh |
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47:15 | model that makes so the virus infected , for example, as the virus |
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47:21 | going through its life cycle, It's producing vowel proteins and this and |
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47:25 | and these can be bound up by C molecules inside the cell and go |
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47:30 | the surface. OK. So, in doing that, they then showing |
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47:37 | energy to the body but because they're it on these class one types, |
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47:44 | ? That's what cytotoxic T cells right? So they'll bind and then |
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47:50 | release chemicals. OK? Uh but the basically the end result is |
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47:56 | the cell lying the cell. Uh These things called porphyrins, |
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48:02 | Basically proteins that kind of form a in the membrane causing stuff to leak |
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48:08 | . OK? These brain enzymes are of like digestive enzymes. So |
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48:13 | and that result is killed itself. Yes, it's one of your cells |
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48:17 | it's a virus infected. No I want to get rid of |
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48:20 | Here's the other population. OK. Now, uh not necessarily all virus |
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48:27 | cells may get this, that this happen, but it will for a |
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48:33 | . OK. Um uh But it an important in infection fighting, I |
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48:38 | also started to talk of T cells recognize some types of cancerous cell types |
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48:44 | well. OK. In the same and uh get rid of them. |
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48:48 | uh so again, dealing with inter , OK. Um And they remember |
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48:56 | other one that can do, this natural killer cells, natural killer cells |
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49:00 | also in a little bit different they don't interact with, I mean |
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49:04 | molecules, but they can also kill cells. Ok. So you got |
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49:09 | couple of ways to deal with in pathos. Um And so this other |
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49:17 | , the, the T helper right? They recognize MH C two |
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49:23 | that's your macrophage is B cells, cells. OK. And so uh |
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49:29 | a macrophage and, and acros are cells, right? And so they |
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49:37 | uh as part of their figy tosis , they can combine some of those |
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49:42 | that they chewed up from a chewing a bacterium or a virus or something |
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49:47 | bind up with MH C molecules and to the surface. All right. |
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49:52 | now you can show it to a helper cell. OK. And so |
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49:56 | uh then leads to release of cytokines from the T helper cell um that |
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50:03 | can activate. OK. So what's a macrophage? I think I mentioned |
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50:08 | before. What it is is it's T helper uh type one cells that |
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50:13 | doing this. It's a T So this would be a th sub |
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50:19 | . OK. They're the ones that with uh macrophages and itself. And |
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50:26 | um here's an example. So this be an inactive or re acro |
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50:33 | There's an activated one. So you see how it's mem membrane folds. |
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50:38 | eat pseudopod are greatly, are formed they greatly enhanced, right? The |
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50:44 | , more obvious diagram is something looks this and then becomes, you know |
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50:50 | these pseudo pods like that, So it becomes very pronounced, very |
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50:58 | if you will, right. So pseudopods may indulge stuff, it's gonna |
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51:02 | something that's gonna be much better in than this rustic form would be. |
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51:06 | that's what this activation process brings right? Um, So the uh |
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51:15 | th type two cells we saw those are the ones that interact with |
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51:19 | cells. OK. Um And, activate B cells, the T dependent |
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51:26 | , right? Um So, all , any questions about that? Do |
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51:34 | start to it to your cells? you help your cells? OK. |
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51:38 | So this last bit is the names different types of music. OK. |
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51:46 | there's different types. So let's take look at this question here. |
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51:50 | I think it's gonna be fairly intuitive figure out. But let's look at |
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51:54 | first one. So which one represents vaccination? OK. So you have |
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52:04 | fork reading from top to bottom, ? Uh Naturally acquired officially. Then |
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52:10 | of those has the same subcategories, , passive, active, passive. |
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52:40 | Right. Cutting down from 14 to . All right, let's see. |
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52:56 | is going to be see. Let's . Yeah, artificially acquired because you're |
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53:04 | a shot in the arm. Uh And it is active, |
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53:08 | Your bo your body is responding and producing antibodies. So that's an active |
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53:13 | . OK. So what about in ? OK. OK. 854. |
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53:54 | . So basically gonna be the opposite , of um vaccination. So what |
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54:03 | both gonna be active processes uh but not naturally a required. All |
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54:07 | So it's gonna be uh a active process then uh let's try one |
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54:14 | OK. And embodies by a OK. Position of an and bodies |
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54:23 | think that this is, yeah, , everybody knows this process. So |
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54:55 | acquired passive. So basically, if , if your body is making the |
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54:59 | , making the antibodies active, if are not having to do that. |
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55:04 | if you get to go get a of um uh Igigg which you can |
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55:10 | um that of course is uh artificial passing, right? So, um |
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55:18 | the uh processes here we just mentioned are you using them? Are you |
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55:25 | , are you being given, being to you? Uh How are you |
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55:29 | them? OK. So um so , you know, you should |
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55:35 | be able to contrast both sides with B cell functions. T cell |
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55:41 | um antibody formation, the plasma memory , uh hormone selection process, uh |
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55:49 | secondary um uh antibody response and then t help or T TT cell um |
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56:00 | is it for we'll do 15, time we have 15, next week |
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56:05 | finish all 15, we will see then What? Thank you. |
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56:34 | my |
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