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00:02 You say you? All right we'll get it started despite the block

00:47 the middle of the screen. that's where we're at underneath that

00:52 Ok. So we are gonna be here in a couple of minutes.

00:57 . So, um, so, , we have a quiz tomorrow,

01:07 quiz. Um, and I answer you on Monday, uh, today

01:13 gonna finish up 17 and the next starting to, uh, 15,

01:21 last part of this. Ok. , the last part of this.

01:29 . Um, uh, microbial Ok. So we'll have plenty of

01:34 to finish that up next week and , uh, uh, then it

01:38 next unit, the last unit week and then they, uh,

01:41 there is still a ways away. , uh, you know, two

01:45 . So remember that the schedule opens , I guess, uh, technically

01:50 midnight. So this morning. uh, if you need to get

01:56 slot, uh, or slot then guess you could be up at

02:01 Ok. Um, let's see. , oh, it's just not

02:07 Ok. Still going. So, , anyway, we'll stop. So

02:10 gonna start with, um, third question. OK. You may

02:14 . If you've gone through the you may know it may not.

02:17 OK. We'll work around it. , but let's look at this

02:22 It almost placed it right. Let try again. Come on. All

02:28 , let's try this. OK. gonna do like that now. T

02:37 on. Uh Yeah. OK. ? Uh I don't know what the

02:49 this is. OK. Um All . Let me, all right while

02:56 answering the question. Let's see. , thank goodness. OK. All

03:02 . So going to weird spacing that how I could get around the block

03:06 . So secondary immune system response. that do a memory B cells

03:13 Is that what they do or can do that? A Glutin Nation Company

03:18 Cells by antibody that true or false Cytotoxic T cells. Is that what

03:25 do? OK. So we will all this today. OK. So

03:31 get through these. If you're not what they are, we will hopefully

03:34 by the end today. Um Let's see. I'm sorry, I

03:42 to open the pool. So if answer, try it again. Um

03:49 . But there uh so um we're on this so kind of a uh

03:57 a little bit. We started this uh at the end of last

04:02 So um the that of new So remember that's the third line of

04:07 , right? Um Your innate immune , physical chemical barriers. Um Different

04:14 types involve um processes involve fever, et cetera. So, um non-specific

04:24 they call it uh Here is more because it involves binding between molecules specific

04:31 between molecules. And so that's what about uh the effects of the adaptive

04:37 system. So that's what we'll discuss . And the false answer here is

04:51 yeah. Uh A gluten a clumping , that. No, that's

04:57 Sorry go. OK. The false is um so A is true.

05:04 . Memory B cells. Um That's uh are built up. That's part

05:09 the vaccination. Uh Outcome is ultimately lots of memory B cells um

05:16 they can bind to both antigen and cells at the same time.

05:21 We'll see that very quickly here. A rotation is clumping of cells by

05:27 . OK. So toxic T cells with intracellular pathogens, not electric cell

05:34 , that's the fault state. Um So cytotoxic T cells interact with

05:41 cells. So virus infected cells, example, can be detected by cic

05:47 cells and gotten rid of, So the B the B cells would

05:52 with extra cellular pathogens through antibodies. . So let's uh so we'll cover

05:58 these here today. Uh So we went through kind of an overview

06:04 the whole process here that immune The key thing is and that's what

06:10 response to. OK. So it's a, there's a recognition component.

06:16 de a detection component, a recognition and then uh a recognition and binding

06:25 then that brings about various effects. . So we went through uh so

06:30 these two halves here can be uh can associate basic two basic functions.

06:36 is the humoral immune system. The cells uh respond to extra C of

06:42 . OK. So antibodies do their outside of cells. They can't go

06:46 of a cell and buy an an . They have, they're external intercellular

06:52 are dealt with by cyto topic T . Uh T helper cells have a

06:58 of different roles and we'll see how develops today. Uh One of

07:02 one of them is to interact with cells to activate them. OK.

07:07 is to interact with macrophages and dendritic . OK. And um these uh

07:21 part of the remote, we call things. Um for short A

07:28 which means antigen presenting set. So are cell types that can, that

07:33 both be part of the innate immune and baby supplies. Uh but also

07:38 of the interact with the adaptive immune and work with certain T helper

07:42 OK. So there are unique cell in that way. So that uh

07:48 can work on both sides. Um uh cell we'll go through these.

07:54 so the other thing to remember is uh antigen epitope, right?

08:00 antigens are on the surface of a . OK. And um they will

08:07 , they can be a number of um molecules, typically, proteins,

08:12 can be like proteins, carbohydrates, cetera um that are on the periphery

08:18 it can be, it can even a Flagel. Ok, a cell

08:21 , a capsule, uh outer membrane a ram negative, et cetera,

08:24 cetera, uh viral proteins on the . So, uh these are the

08:29 antigens interact with antibodies interact with. so we are closer to the finding

08:36 than an antibody. Oh All look that up, there will be

08:42 area within that antigen should engrave red where it actually binds to. So

08:49 call that the epico right. So the, if the square here is

08:54 antigen, right, then this smaller inside is what it's binding to.

09:01 we call that the epitope. Um So uh so as we look

09:08 further at antibody structure, OK. antibodies basically think of it as a

09:12 , right? So letter Y with couple extra things on it.

09:16 So um there is regions that are what they called constant regions.

09:24 Um And variables. So these change antibodies to antibody out here,

09:30 This is the antigen binding sites. ? They're called variable sequence. They

09:36 in amino acid sequence and it depends what they bind to, right.

09:40 your ability to bind all types of and there's like the the number of

09:47 you have that can respond, you theoretically respond to like got into the

09:53 it's a super crazy number. It's a 10 to the 15th or something

09:58 that. Uh Possible types of different that are out there. So remember

10:03 have engines that are part of a like pathogens and viruses and protozoans and

10:09 and whatnot. But I also remember like um different chemicals can be

10:15 be an antigen, uh pollen. , I all aware of that in

10:19 , uh ragweed, et cetera. these kind of things serve as uh

10:23 antigen that can stimulate your immune Sometimes not in a good way if

10:28 got allergies on it. So, but uh the, the in

10:34 you have, so you have five here. IgD and IG stands for

10:40 . OK. So immunoglobins uh GDEM uh A OK. Now, uh

10:48 something you need to know, but for your own knowledge. So you

10:53 identify a G ad A E uh , and a based on similarity in

11:02 constant region. So in other all IG Ds are gonna be the

11:07 in that area. All IG DS the same. So that's what,

11:11 , that's how you can identify each . Uh What does that, what

11:15 that part of the antibody look And so each class will have its

11:20 sequence there. OK? And they , and they all be the

11:24 OK. But of course, they'll out here. OK? Because you

11:29 , you can have thousands of IgG and some respond to this engine,

11:36 respond to that engine. So they're be different in the, in the

11:39 and body parts. OK? Uh so what else? So we

11:44 So as I mentioned in the so these parts or that are variable

11:50 to antigens, of course. But then this part combined with a

11:54 , right? So this can be um a macrophage for example, well

12:00 a macrophage but it can be a it can be a B cell for

12:05 . OK. Um That's how these actually work. They have antibodies in

12:10 surface, they find the hands. . So uh that is true.

12:14 you can have both those but remember it could be I'm just uh brain

12:20 . It could be a macrophage because the optimization process, right? Optimization

12:27 when a macrophage binds this part and these parts are stuck to the pathogen

12:32 take the whole thing, right? the optimization. So yes, uh

12:37 of them be cam as well. the point is and and some antibodies

12:40 do this, they can find the and they can bind the other other

12:44 to itself. That's what we call FC portion, right? So an

12:49 portion, a cell can have a FC receptor to it right now.

12:57 Let's see. OK. So it's a couple of questions that relate to

13:02 function. So we're gonna go through five different classes and then um uh

13:10 of see what their functions are, get a little more information on

13:14 Uh These, these are located sometimes different body fluids. Um they can

13:21 different functions, of course. Um here it's asking antibodies found on mucosal

13:27 in mucosal secretions and functions to interfere pathogen adherence. OK. So this

13:35 part of that. Um you could this part of the chemical barrier,

13:40 . So remember that your physical skin uh mucus membranes, they have

13:46 secrete some kind of fluid and the will contain different types of antimicrobials,

13:52 ? It can be something lysozyme uh this particular antibody can be in there

13:58 well, right? So let's speed this up a little bit.

14:06 what can happen? 10. Let me see. OK.

14:21 All right. Yeah, it's gonna IG A. So IG A is

14:27 uh one of the big um major ways of pathogens are able to stay

14:34 your body is they adhere to your membranes. So that's kind of where

14:39 live in many cases. So um meningitis organism, uh lots of respiratory

14:46 uh that enter through your nose or throat, uh need to have mucosal

14:51 . And oftentimes they have ways to they need to stick to your,

14:56 these uh membranes and if there's an A, it can bind to it

15:00 then block its ability to stick that a good uh defense for those types

15:06 pathogens. Um OK. The Hallin . OK. Is the specialty of

15:16 Pyramid. Pera Pitta me, excuse . Um I mean, like,

15:22 we'll learn that um industry is the choices and as are shown the uh

15:31 antibodies can um just be in the form, the singular Y form.

15:39 But some can group together like this not always in groups of five,

15:45 in groups of two. So IG can actually do that. OK.

15:51 um uh and that kind of it , it enhances their funk,

15:57 So it used to have, they two sites, right? We're just

16:02 this form, you'll have two engine sites. 12. But if you

16:11 , all right, now you can 41234. So it kind of increases

16:19 ability to bind, to bring, bind up uh energy. OK.

16:25 uh even more. Oops, even uh timer. All right.

16:39 right. This thing closed prematurely. fault. Let's try it one more

16:43 . Sorry. This is um there go. So yeah, it's gonna

16:50 the function of those types of not all of them do it,

16:54 some can form these multiple groups OK? Um All right. Counting

17:15 . So one, all right, we go. So uh it

17:23 I believe that's m correct. So is forms these uh types of

17:30 And so what happens is they can up a bunch of cells at one

17:35 um having basically 10 and your binding . Um And so the last one

17:43 is about this function of, of so that can uh certain antibody types

17:55 their function when sitting on top of cell, right? Others can be

17:59 floating, OK? Igaigm. Um others only work, I just gave

18:07 a hint there others only work and sitting on top of the cell and

18:12 how they function. OK? We down to nine. All right.

18:28 this is going to be um IgD IgE. So it's actually uh C

18:37 D. OK? So both of work I sit and talk about uh

18:45 yeah, all time. OK? we'll talk about that now. So

18:49 I just mentioned earlier the IG right? So again, there in

18:54 percentages you don't need to simply memorize percentages. But uh ID A is

19:03 is not need and percentages that they're in blood. OK. So it's

19:07 because it's mostly found in the culture , right? Uh your nose,

19:12 throat, you know, body cavities aligned with the mucosal membrane,

19:18 And so what they do is what's a neutralizing function. So, neutralizing

19:25 uh by binding to the microbe, ? They can effectively prevent it from

19:31 cells and binding to your cells. . That's what neutralizing antibodies do.

19:37 . That's what uh COVID vaccine promotes antibodies. So, by coding the

19:43 , the virus can't stick to your or your respiratory tract. OK.

19:49 And so IgG is typically what they the workhorse antibody. It can,

19:57 uh it typically shows up, it's the main, main one in

20:03 to a, a pathogen or in vaccine. Uh versus IgM and IgG

20:09 large numbers. OK. And they a number of functions to um be

20:16 Selman. So help with oc cytosis activate complement uh the neutralization of

20:22 They have a lot of these functions uh that are important in fighting

20:26 OK. Um So they're gonna be , at the highest concentration in the

20:31 . OK. The uh IgD is of those that works by sitting on

20:36 of a cell. So they would on B cells and B cells uh

20:42 the ones that produce antibodies. So hands and binds to these antibodies on

20:49 surface that will stimulate the B cell produce more antibodies. OK.

20:55 um B cells typically have IgD A have IgM on their surfaces.

21:02 And that's how the engine binding leads them, doing their functions.

21:09 Um And so because B cells are found in lymphatic fluid and lymph tissue

21:18 outside the blood, you don't see at very high concentrations in the

21:23 they're sitting on the B cells which not in the blood out in the

21:27 system. Ok. Um IgM, the one that forms the P

21:33 So it will form. So, is clumping. Autin is the clump

21:39 together. OK. And so um what it can do by by doing

21:45 agglutination function, it reduces the numbers infectious units, the body has to

21:52 with. So it kind of concentrates . So if we have, for

21:55 , 10 pathogens, uh when this forms these um P forms,

22:03 Uh with 10 binding sites, it can clump up a number of

22:09 microbes uh at the same time. now you've reduced 10 infectious units on

22:14 left down to one that the body to deal with. So it's an

22:18 function in terms of uh concentrating and dealing with these, dealing with an

22:23 agent like this. OK. And lastly, IgE, right. So

22:28 , they're found low amounts because basic are typically uh not in high concentrations

22:34 the blood right there in the surrounding . And so uh those that have

22:40 allergies or hypersensitivities or hay fever, like that. You can blame this

22:46 here, mass cells or basal pills IgE on top that binds the engine

22:52 sometimes it works too well. You a hyper response and that's what causes

22:57 of, of, you know, eyes and these kind of things.

23:01 . An inflammatory response can result. . So uh but so bays mass

23:07 , there are things kind of to various types of chemicals, like I

23:11 , in response to inflammation and, these kind of things. Ok.

23:17 ok, so those are the five . And so um so your

23:22 and again, so remember that these are released that collect the term

23:26 right? For these things work on immune system cells. OK. Um

23:33 right. Any questions at that My hand hand about the structure

23:38 OK. Uh So let's look at question. OK. So this

23:46 so now we're gonna get into more cell function from T cell function.

23:52 . So uh B cells, most human immunity, T cells mediate certain

23:59 . B cells can differentiate into antibody plasma cells. A single coronal population

24:07 plasma cells can produce antibodies to many ops. OK. T cells can

24:13 kill infected host cells but these cells cannot directly kill cells. OK.

24:31 . OK. That OK. Let's see. Koo. OK.

24:56 the sides to me, right? So um let's just go to the

25:09 up. So T cells can directly infected host cells. Um The B

25:16 themselves cannot directly kill cells. That's . OK. So T cells like

25:21 cytotoxic T cell um can kill an cell. These cells themselves don't kill

25:27 but they can, they, their is through antibodies on their surface,

25:32 ? They don't actually kill anything but antibodies they produce can lead to different

25:37 . Ok. So this is Um The single of population of plasma

25:46 can produce ops to many different or produce antibodies to many different ops.

25:51 Is that true? Yeah. Image uh BTS. Anybody is false.

26:00 think it's hot? Don't be afraid name is false. My name is

26:10 . Yes. Why? Oh Come on. Why? I know

26:16 Jesus tells me what's the operative words ? What is a, a colonial

26:28 is? What? They're all if you have a clone, you're

26:35 what the same, you're identical. . Um They're the same. So

26:44 single clonal population of plasma cells produce . Too many different ops. So

26:49 they, if they're all the are they gonna produce different antibodies?

26:56 clones, they're gonna produce the produce , that same. Yes. Say

27:04 be confident goodness, the same So that's what a clone, a

27:10 population is. They make, they the same function, same thing.

27:16 A and so a clonal population will antibodies to only one epitope. That's

27:21 basis for your antibody response to vaccine for, for an infection.

27:29 So that's the false one. Um cells can differentiate into antibody supreme pasmo

27:36 of, of course, that's And that's true. OK. So

27:43 all right. So let's see how happens here. OK. Question.

27:51 , I got batteries. Hold All right. Well, that's doing

27:54 . Let me turn this on. . So, um, with humoral

28:04 immunity, we're talking about B cells their function. Ok. So,

28:19 , remember though they deal with extra pathogens? Ok. So, let's

28:38 . All right. Uh So um, so there's two pathways,

28:44 one that's most common is what you're see here on the screen. That's

28:49 um uh the T cell T cell and dependent process. OK.

28:57 in other words, it requires the cell requires a T cell to be

29:01 of the process. OK. The part we'll talk about next is

29:06 The B cell that does not require T cell to activate it.

29:10 So um so what happens is androgen an by an by will be on

29:17 of the B cell. It can a uh IgD and IgM sitting on

29:23 and binding an antigen to. It occurs as well as B cells will

29:30 these antic fractions. OK. And um so I remember B cells are

29:37 cells, dendritic cells and um uh have these uh uh class two types

29:47 MH C molecules. OK. And they'll show antigen. So B cells

29:52 be antigen presenting cells. OK. so they use that function to interact

30:00 the T cell. OK. So that antigens, T helper type two

30:07 respond. OK? And they in activate it into a antibody producing plasma

30:16 through the act in the B turn it into a plasma cell as

30:22 as into memory B cells, So both are the result of this

30:27 . OK. So again, this what's called the T dependent antigens,

30:32 ? And these tend to be the common ways to activate a B

30:36 OK? To involve TT helper cell it. OK. And so,

30:43 so the uh so the uh other that happens and uh let's see this

30:53 next. It's in a couple of , but there's a process why a

30:57 independent type doesn't need to help with T cell. And we'll see that

31:01 . But let's look first at this clonal selection process. So, what

31:05 talking about is when an engine is , OK? You're gonna have pools

31:12 B cells, right? Thousands of of B cells, right? And

31:17 each will have antibodies sitting on top each pool will be able to theoretically

31:23 to any energy that's out there. . So that's what this is about

31:28 . This is what clonal selection is you're gonna have. So here just

31:31 it simple. 1234 populations of right? Each one, each one

31:38 itself is a, is a, the same, OK? Is a

31:45 population. So this is one, all have the same anti body that

31:49 to the same antigen, right? is one that has binds to a

31:54 engine. All bind to that same so and so forth. So we

31:57 four groups, you know, your will have thousands of these.

32:01 So um so as an engine comes here is red, so red,

32:07 . Uh presumably it will bind to antibodies of one of these populations.

32:13 ? This this example, it's binding not 123, but number four,

32:18 . So any B cells that that are four in the four

32:22 four C group, OK will bind antigen. OK. And then only

32:29 group then goes on to differentiate. . So they will produce well what's

32:36 clonal expansion. So you have a cells here that then correspond to angel

32:41 divide. OK. So you produce population of clones. OK? And

32:49 they differentiate into memory b cells and cells. So plasma cells are the

32:55 ones that may OK. Uh The of a plasma cell is about 60

33:03 . OK. Then they die, ? The plat the memory cells of

33:07 can last for decades, right? can last 3040 years. OK.

33:14 sitting in your body waiting for the time that the engine reappears, then

33:19 can uh start the producing antibody. what happens is when the when the

33:25 cell get stimulated, then it differentiates a plasma cell and more memory

33:32 OK? And it's the plasma cells won't produce the through the antibody

33:38 So, uh but you know, cells, although they can last a

33:43 time, um some do kind of their what's called immunogenicity over time.

33:51 they're not as strong in terms of to an engine as they once

33:55 right? So that's kind of figures why you need a booster shot every

34:00 and then for certain like tetanus, example, you get a booster shot

34:03 every 10 years or so as well certain other other uh vaccines. So

34:09 is kind of meant to boost up population of memory cells. OK?

34:14 But the um the uh T independent , OK? They don't require this

34:24 via BEA OK? And so the is so I'll jump back to this

34:30 this next thing I'm gonna show you only for explanatory purposes are not gonna

34:36 tested on OK? But it, , it's the only way to kind

34:39 tell you how you differentiate these two . OK? The T dependent engine

34:45 itself requires um energy, of binding to the body of the

34:51 So here's a s what you would a small engine, right? Compared

34:56 a big super big molecule, like a big sugar polymer or

35:01 right? So this is like this called an average sized antigen.

35:05 Typical, typical size, right? what has to happen is because you

35:11 , antibodies can have two binding they interact right in the bond antigen

35:16 they form what's called a B cell . And so this process of binding

35:21 kind of coming together, it's called . Again, don't worry about

35:26 I'm just kind of show you how happens. Uh This then leads to

35:32 MH C molecules showing it also comes the cell and it shows it

35:38 And so this process only happens with dependent uh in the T dependent

35:44 But uh with your more typical size , it's the more common way.

35:50 ? Now another way to kind of those antibodies together, OK, bunches

35:55 them together to act to activate the is to do this, I could

36:02 that. You see this big long , right? So we can bin

36:08 bring together a bunch of the antibodies the surface because it's so big.

36:13 that's what accurate the E cell receptor makes the, the cell able to

36:17 produce antibodies without the contribution of a cell getting into it. OK?

36:25 That's really the basic difference. T , this one and T dependent.

36:32 it's about the size of the OK. And um like I

36:38 the more common is with, you , these regular size, I call

36:41 size, uh typical sizes. Uh can, this can happen, of

36:46 , it does. But uh they these really large ones. It's not

36:50 common, but it you know, happens as well. OK. Um

36:57 Yeah, so the other thing to is that once it's uh activation

37:02 which mechanism you are gonna hang path and memory cells form. OK.

37:07 that really is what forms the basis vaccination. OK. Um Let's uh

37:17 about this. So any questions this ? OK. So uh so,

37:24 talking about vaccinations, this could this could be vaccination, it could

37:28 initial exposure due to va v OK. And so the uh uh

37:37 . So again, this is AAA that occurs over uh several days because

37:46 um your body has to recognize detect it. Number one, recognize

37:52 and buy into it. And that's a time on to that.

37:55 And so uh there's always gonna be time to evolve for that reason.

38:00 you see there you go to an takes about a week right before we

38:05 to see um a response by the well, detectable response. OK.

38:11 so what happens is initial exposure? is the primary response. OK.

38:17 Andrew is introduced whether through vaccine or and uh first antibodies form are,

38:26 IG MS, right? They form the Pinter forms, right? And

38:30 then followed by IGV, as I before, this, this whole process

38:35 antibody formation and, and um uh immune system in general, the ad

38:41 in the system is very complicated. um because you do, they'll talk

38:46 it here. But uh there's a curve for these cells and the energy

38:53 binding. OK. So initially, IG MS aren't that great.

39:00 Uh But because they have the pension , that helps because you can clump

39:04 a number. So even if you , even if the binding is not

39:08 great, OK. But then the that follow. So, so you

39:14 , you can have a B cell . OK. So, all

39:20 And um so it binds antigen and G is short for antigen. And

39:29 this B cell will first produce Well, plasma cells will OK.

39:36 then these will be kind of not super Bindy to antigens, but they'll

39:41 well enough. But then it's kind a learning curve and part of that's

39:44 of continued binding, helps it bind kind of a thing. OK.

39:48 then these cells then switch to OK. So the same B cell

39:55 responded from IgM can also then switch a different antibody type G type,

40:02 ? So what's called um class Don't worry about it, but just

40:07 of showing the versatility of these, these types of cells. So B

40:12 can first do this and then the one can then do the other

40:14 OK. And in the second the IgG tends to be a better

40:20 . So IgGs are are kind of work course as I said they have

40:24 of different functions. So, and get a big response from them as

40:27 see in the blue line there. of fact. So, so your

40:32 so in your primary response, it a long while because you're just,

40:37 your first exposure and again, your system cells have to find it,

40:43 it and then do their thing that time, right? So, but

40:46 you're doing in that in that right is making uh plasma cells and

40:52 b cells. OK? And memory cells you're putting away storage so you

40:58 call on them later. OK? positive cells will be the ones pranking

41:03 and will live for about a couple months. OK. So if you

41:08 um second exposure, whether it's through uh an infection by the same pathogen

41:15 a booster shot, right? Then response is much quicker. The timeline

41:21 as long, right? More And so uh and that's because you've

41:27 memory cells ready to go, You form those in the primary

41:32 Now they're ready to act and energy long boom. And you're forming plasma

41:37 to make antibody and you form more cells. OK? So that's why

41:42 response is much quicker because they're, primed and ready to go.

41:48 Um And of course, that's obviously nature of white and booster shot is

41:51 really enhance that response and make lots memory cells OK. Um, now

42:02 uh, and some vaccines do this than others and we'll talk about

42:06 We'll talk about vaccines in, in little bit of detail later. But

42:12 vaccines are better at this than others terms of producing lots of good antibodies

42:17 a big response. And there's reasons that. We'll, we'll talk about

42:21 later. Um, any questions about ? All right. Uh Right.

42:29 so what ha what are the what are the end results of the

42:33 body? And an and B? . Well, there's multiple, we've

42:36 a couple for the the hallucination the bindings that reduces numbers of,

42:42 infectious units um to by clumping and , the nature of having two binding

42:49 , right? Even better if you form that, that Pru or like

42:53 the IgM can uh ization. We've about that before, right? Enhancing

42:59 cytosis neutralization we mentioned earlier. Uh know, of course, remember that

43:04 are uh can you can form antibodies toxins or like tetanus. Um And

43:10 if and toxins depend on binding to cell and getting into the cell and

43:16 damage. So if you can prevent , and that's what neutralizing an bodies

43:20 . They cope pathogen or the And now these things can't bind to

43:25 cell and do their damage. Basically, you're neutralizing the pat think

43:31 it that way. OK. Uh compliment, we've talked about that

43:35 So anybody can do that. That's classical pathway. And then um then

43:44 the, this one right here. I think I may miss this earlier

43:51 this is uh A DC C for uh standing for antibody pendant cars

43:58 Uh C mediated brings a number of to the party cytotoxicity grows up thinking

44:04 death of the, in this parasite. These are for ABC C

44:11 for a large parasite. It's like large worm. Uh protozoan, what

44:16 you amoeba? What have you a large? Ok. Not your bacterial

44:22 , your viral size, but my . And so uh so to bring

44:27 down, that's that big is gonna a collective effort, right? Gonna

44:33 lots of cells. And so the to do that is to use antibody

44:39 your mechanism from antibody to the parasite bind the cells combined with the combined

44:48 that FC part of the antibody. so things like Eoin Il can do

44:54 . So from your ails are toxin cells. So you get as much

44:58 these together hand body finding, I collectively they release a toxin, overwhelmed

45:07 can come in as well, releasing chemicals. So uh it's a way

45:12 have cells stick all across this parasite antibodies and then together kill it.

45:19 . Um So all these result in you know, chilling of the microbe

45:25 uh not allowing to attach, which can you can get rid of it

45:29 the system this way, uh killing here, of course, in ox

45:33 clumping it, this can uh this bind up bacteria and uh maybe macrophages

45:40 things can come and involve them So the end result is uh

45:44 to get rid of the passengers, , OK, in different ways.

45:49 , um so again, this thing is these are all all extracellular.

45:54 all these are all extracellular pathogens that being dealt with here, T cell

46:00 where we talk about dealing with infra , right? So uh speaking of

46:06 cells, so here is cytotoxic T . So these uh interact with your

46:14 that may be potentially infected. Uh differentiation between T cell interaction with your

46:24 is through the MH C molecules. ? And so remember macrophages, they

46:31 cells, b cells have MH C , right? And that's what T

46:36 cells interact with. Pic T cells with MH C type one,

46:43 So remember if you're not a B , you're not a micro or you're

46:48 a dendritic cell, you're basically every cell in your body, right?

46:52 cell, liver cell, neuron, cell, bladder cell, whatever,

46:58 ? Your body cells, uh if become infected, then potentially a T

47:04 can find it and kill it. . But they can only do that

47:09 the infected cell showing what's infecting it the body. That's where the Mh

47:15 model that makes so the virus infected , for example, as the virus

47:21 going through its life cycle, It's producing vowel proteins and this and

47:25 and these can be bound up by C molecules inside the cell and go

47:30 the surface. OK. So, in doing that, they then showing

47:37 energy to the body but because they're it on these class one types,

47:44 ? That's what cytotoxic T cells right? So they'll bind and then

47:50 release chemicals. OK? Uh but the basically the end result is

47:56 the cell lying the cell. Uh These things called porphyrins,

48:02 Basically proteins that kind of form a in the membrane causing stuff to leak

48:08 . OK? These brain enzymes are of like digestive enzymes. So

48:13 and that result is killed itself. Yes, it's one of your cells

48:17 it's a virus infected. No I want to get rid of

48:20 Here's the other population. OK. Now, uh not necessarily all virus

48:27 cells may get this, that this happen, but it will for a

48:33 . OK. Um uh But it an important in infection fighting, I

48:38 also started to talk of T cells recognize some types of cancerous cell types

48:44 well. OK. In the same and uh get rid of them.

48:48 uh so again, dealing with inter , OK. Um And they remember

48:56 other one that can do, this natural killer cells, natural killer cells

49:00 also in a little bit different they don't interact with, I mean

49:04 molecules, but they can also kill cells. Ok. So you got

49:09 couple of ways to deal with in pathos. Um And so this other

49:17 , the, the T helper right? They recognize MH C two

49:23 that's your macrophage is B cells, cells. OK. And so uh

49:29 a macrophage and, and acros are cells, right? And so they

49:37 uh as part of their figy tosis , they can combine some of those

49:42 that they chewed up from a chewing a bacterium or a virus or something

49:47 bind up with MH C molecules and to the surface. All right.

49:52 now you can show it to a helper cell. OK. And so

49:56 uh then leads to release of cytokines from the T helper cell um that

50:03 can activate. OK. So what's a macrophage? I think I mentioned

50:08 before. What it is is it's T helper uh type one cells that

50:13 doing this. It's a T So this would be a th sub

50:19 . OK. They're the ones that with uh macrophages and itself. And

50:26 um here's an example. So this be an inactive or re acro

50:33 There's an activated one. So you see how it's mem membrane folds.

50:38 eat pseudopod are greatly, are formed they greatly enhanced, right? The

50:44 , more obvious diagram is something looks this and then becomes, you know

50:50 these pseudo pods like that, So it becomes very pronounced, very

50:58 if you will, right. So pseudopods may indulge stuff, it's gonna

51:02 something that's gonna be much better in than this rustic form would be.

51:06 that's what this activation process brings right? Um, So the uh

51:15 th type two cells we saw those are the ones that interact with

51:19 cells. OK. Um And, activate B cells, the T dependent

51:26 , right? Um So, all , any questions about that? Do

51:34 start to it to your cells? you help your cells? OK.

51:38 So this last bit is the names different types of music. OK.

51:46 there's different types. So let's take look at this question here.

51:50 I think it's gonna be fairly intuitive figure out. But let's look at

51:54 first one. So which one represents vaccination? OK. So you have

52:04 fork reading from top to bottom, ? Uh Naturally acquired officially. Then

52:10 of those has the same subcategories, , passive, active, passive.

52:40 Right. Cutting down from 14 to . All right, let's see.

52:56 is going to be see. Let's . Yeah, artificially acquired because you're

53:04 a shot in the arm. Uh And it is active,

53:08 Your bo your body is responding and producing antibodies. So that's an active

53:13 . OK. So what about in ? OK. OK. 854.

53:54 . So basically gonna be the opposite , of um vaccination. So what

54:03 both gonna be active processes uh but not naturally a required. All

54:07 So it's gonna be uh a active process then uh let's try one

54:14 OK. And embodies by a OK. Position of an and bodies

54:23 think that this is, yeah, , everybody knows this process. So

54:55 acquired passive. So basically, if , if your body is making the

54:59 , making the antibodies active, if are not having to do that.

55:04 if you get to go get a of um uh Igigg which you can

55:10 um that of course is uh artificial passing, right? So, um

55:18 the uh processes here we just mentioned are you using them? Are you

55:25 , are you being given, being to you? Uh How are you

55:29 them? OK. So um so , you know, you should

55:35 be able to contrast both sides with B cell functions. T cell

55:41 um antibody formation, the plasma memory , uh hormone selection process, uh

55:49 secondary um uh antibody response and then t help or T TT cell um

56:00 is it for we'll do 15, time we have 15, next week

56:05 finish all 15, we will see then What? Thank you.

56:34 my

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