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00:10 Yeah. Hey looks um let's get here. Um Let's see. So

00:31 sent an email yesterday basically telling you to do. So we got weekly

00:39 again this week Mastering next Monday, gonna finish up 16 today. Um

00:48 the second part of the innate immune , Thursday is uh that system that

00:54 do a bunch of questions around that . We'll do, we'll start with

00:59 very beginning of Chapter 17 at the today just to kind of go over

01:06 . Um The schedule, remember the opens this friday. Okay, so

01:13 a spot. Um exams still still couple weeks away, two plus weeks

01:20 . So um certainly we got questions , you know, material, obviously

01:26 me know combining office hours, email have you. Okay? Um Then

01:34 let's see. Next week we'll finish Um you get three and start,

01:41 know, for the following week. . Although we may may start some

01:48 it here, depending on, you , I'm thinking that we only have

01:53 come, so class ends on thursday 1st I think. So we may

01:58 have to have class that day if keep on schedule. So um

02:04 um the other thing was midterm so I have calculated that will be

02:12 in the morning. Um I'm just that, but will be posted in

02:16 morning. So I didn't do all heavy lifting, I would do if

02:20 was a final grade, but it's fairly close estimate. Okay, I

02:26 go through. And so it's like the forget the top the top

02:33 clipper sports or what are averaging, didn't do all that but it's still

02:37 gonna be close enough estimate for what need, what you need. And

02:42 it also includes the extra credit from I assumed I was gonna fill out

02:46 survey last evaluation til you get expert that so that's figured in. Um

02:51 the kicker is appeared in it but can always just add a point or

02:55 too great. So a little bit estimate for now and uh and you

03:00 look on, I'll put it in email ahead of time where I

03:04 Um but it's just it's really like exactly in the syllabus just taking your

03:10 on blackboard and just fall in step . Okay. Um And uh the

03:20 um remember but uh um oh the , so we described as a numerical

03:30 obviously. So you're gonna compare that to the scale. It's in the

03:34 on where it talks about the all to that scale in the email as

03:40 . So that's what you're gonna compare two to get a testament of your

03:43 grade. Okay. Um Alright. yeah so watch out for that and

03:48 guess I'll send an email out ahead that in the morning. So um

03:55 see. So I don't think the is the 16th, is that

03:58 I think the 16th don't hold me that but I just want to give

04:03 that information to make a decision if if you're thinking about dropping.

04:09 Um and so you can easily figure because the question then becomes what do

04:15 need to make an exam? Three four blah blah blah. Right so

04:18 can do that yourself. Just plug the plug in 100. Right?

04:22 that will give you at least the upper range. Right? So that's

04:27 enough to just follow the steps that in the that are in the

04:31 I mean in this office. Okay um the okay questions just let me

04:39 . So let's uh we're gonna do start with two questions and then a

04:48 bit of a recap of last Okay so let's start here. So

04:55 talked about all of these last Okay so take a look. Um

05:04 is the true statement. Okay and not A. D. D.

05:11 it's uh F. If and on . On F. There you're not

05:49 see that on an exam where you to identify visually what cell type but

05:53 just threw it in for grins. captain down. MS. All

06:40 calm down from six 54. Yes is. See uh so bas a

06:55 the primary of Vegas an excel type neutrophils initially then followed up by

07:04 Um Two like receptors, they don't anything right there, not a cell

07:10 , a surface molecule that binds to champ. Right and that initiates cytokine

07:16 . And the alarm bell. So receptors are the alarm system so to

07:21 . Uh pam's is correct. That's that is. The person's that's involved

07:30 think of that as facilitated Figo So it's 20 past was coated with

07:37 are complemented and that's taken in for that pathogens that aren't easily oxidized.

07:44 Estonians are made to them and makes melon killed. So that's that's your

07:50 on your cells and tissues. It's self. Okay so we'll touch on

07:55 again here in a second. Just a recap lymphocytes these are actually um

08:02 . They have that weird lobed um . Okay so those purple blobs are

08:10 D. N. A. Um But again I'm not gonna just

08:15 this in it's not gonna see images you have to identify the cell type

08:22 on just the email so don't worry that. But uh maybe a nursing

08:27 . You have to do that but here. Um Okay one more question

08:31 we do some content here. So virus infected cells might be dealt with

08:37 . So I remember the exercise packages patterns and systems. Systems to deal

09:12 . Mhm. Okay. Timer Okay counting down six. Okay it

09:54 going to be natural killer cells. so those and cell type we haven't

10:02 talked a little bit about it but t cell types what are called site

10:11 toxic T cells put them in natural cells deal with infected cells. Um

10:19 , so a little bit of recap . So in the community. So

10:23 what we're doing. Talking about Right? So think about its 1st

10:26 2nd line defenses. First line physical barriers to remember your physical barriers of

10:32 skin. Because membranes also secrete secretions those service chemical barriers that can take

10:40 . I'm is very common. Um simply the nature of the secretions may

10:46 sold to the city that that it be a deterrent. Um second line

10:53 but also the first thing I remember is your microbiota. So that also

10:57 part of second line are typically cell processes um So inflammation. We'll talk

11:04 today fever. These are processes of can involve cell types for sure.

11:11 but uh specific cells uh that things that. So various types of um

11:24 to to counteract pathogens. So we in a question about champs.

11:30 So these are these are the peripheral of pageants out of membranes. So

11:39 the gel. Um so things on external part of pathogen. Okay.

11:46 combined uh manufactures to contradict the cytokines sells, they're gonna bring themselves to

11:54 site of infection. They can have defects. Okay. Um uh we'll

12:01 a lot about cytokines today in the of inflammatory response. There's a lot

12:05 those uh here in the inflammatory response do different things. Okay? Um

12:14 there's okay, different stereotypes going through types. Each have different roles and

12:21 skills are mostly kind of releasing release different types of chemicals inside of kinds

12:27 in inflammation and other processes used to figures of times, but their role

12:33 also toxin producers, but to work really deal with large pathogens. Modern

12:41 , differentiated macrophages, uh panic The lymphatic system is about protecting its

12:49 ingested microbes. Um your tissue can quite dense in certain parts of your

12:56 , and these are full of B cells, T cells to help

13:01 infection. Um and then uh let's here. So then uh because a

13:09 this optimization. Right, So, talk about these today. We haven't

13:12 there yet, but just quickly on . So this is important because it's

13:21 ability to recognize something as an entity be in your body can only occur

13:30 your body knows to differentiate between what's and what shouldn't be there. And

13:37 course, occurs through everything occurs through occurs through molecules of some type.

13:42 so self antigens are kind of like barcode to identify yourselves as europe.

13:48 , so if something comes in that have that same barcode and that's a

13:52 . Okay, And that's what can the immune system cause different effects.

14:01 you have, that system is broken into two types, depending on the

14:06 type. Okay so I always do first because it's the easiest it only

14:11 three types. Right? It has cells macrophages and dendritic cells. So

14:16 just cell types that are called antigen cells. They show energy to the

14:22 . Okay. That can then Different cells respond to them. Uh

14:27 everything else that's not in that group A. M. A.

14:31 One is basically all your body Okay not red blood cells. They

14:36 their own system. That's the EOS their hand system. Okay. Everything

14:42 that's not the type to is a one. Okay. And so um

14:47 so we'll see as we get into adaptive immune system you have certain of

14:53 cells interact with these types of self . Others interact with these. Okay

15:00 that's what kind of differentiates their function . Talking about different types of t

15:06 interact with these two. Okay so know I'll keep repeating this and it

15:11 become clearer as we go through. So that they may see engines here

15:16 just on the surface of the The originally inside the cell of course

15:21 can then they can make the molecules that are synthesized and they combined a

15:30 piece. Right? That's a piece a virus or of another bacterium.

15:41 bacteria can enter into the cell and out. So maybe it's a piece

15:44 that and it goes to the surface ? And now the immune system can

15:50 A G is for an engine can oh here now it goes to the

15:55 and now it's shown to the body it's inside is invisible from the outside

16:02 other system cells can respond. The cell can respond what have you.

16:07 . And that's how you can find what's going on in terms of your

16:11 system or you can have cells like . Right. And so um you

16:17 infected cells cancer cells can have different on their surface. Okay. Maybe

16:23 lack MHC molecules altogether. That's what killer cells. So because that tells

16:29 body it's it's not normal it's abnormal to have MHC antigens on the

16:34 So sometimes infections like a viral infection all. But some can cause these

16:40 to the surface. Certain cancers. cancers can do that. And so

16:45 what a looks for. Uh there's type. Don't worry about this

16:51 What was called the side a toxic . Cell. Okay, these two

16:58 for uh infected cells are actually And again okay through their MHC one

17:08 that's the energy in there. And it varies and in effect itself can

17:16 on the viral type and it will different responses. Some maybe like this

17:23 and sort of toxic natural killer cell be on the lookout for or maybe

17:27 doesn't have that response and it and does have MHC engines on it.

17:31 they show a Part of that affecting as an on the surface. So

17:39 have T cells can recognize that. talk about that in 17. But

17:44 from while we're here worth mentioning to point is, you've got multiple ways

17:48 deal with different types of infections. , so this is a that's an

17:54 sailor cellular. Yeah. So, on the inside in try cellular

18:13 So you have to have a way deal with those and those that are

18:15 the outside. So when you call here, foodborne illness, right,

18:21 . So you have both obviously both affect you and ways to deal with

18:26 . And we do we have specialized that can deal with each type.

18:29 , so you do have a lot defenses. I mean, have you

18:35 earlier the physical chemical barriers accepted. , we got a lot of stuff

18:38 on that can that happens. Uh gonna happen that can be triggered in

18:42 course of an affection. Ok. is all good for you. Um

18:47 questions about this self engines. All right. Um okay, so

18:53 lastly optimization. So remember a nutritional as part of the process can also

19:04 . So this is a kind of writing, but that's a total like

19:08 T. L. R. For . Right. And so that can

19:13 cannot only engulf and ingest and break down. But in the binding part

19:19 can you have a times to alert cells infection. Um these uh once

19:28 gets crunched up right? So there's fake ozone refuses with a nice

19:33 Right? And so then it gets that material can exit. So but

19:39 we have this will have MHC Okay, a macrophage if that's what

19:44 is would be a type two. so it will bind to some of

19:49 particles. Okay then show it C , Auntie Gin and then this would

20:00 um the part of a virus or crunched up in there and show it

20:06 the body and now it's visible to cells of the immune system.

20:12 That's what that's what engine presenting cell . Okay shows whatever digested to the

20:19 to the immune system can respond if . Maybe it's nothing. Maybe it's

20:23 there's no response because it's not a but maybe it is. So that's

20:28 to be determined by the cells that with. Okay and then here is

20:32 optimization right? We have the pathogen and it's coated little y y shape

20:42 or antibody. Okay so antibodies binding in and that's what it's doing.

20:49 so you have these these parts of antibody bind to the pathogen.

20:59 This part combined to a cell like macrophage to have different binding parts.

21:09 that's so optimization accounts for those pathogens aren't easily famous, it ties because

21:15 slippery like a thick capsule or So we have antibodies to it or

21:21 the other one. So they're both complement and antibodies coat to sell.

21:27 makes it easier to bring in the fight. The specific cell can bind

21:32 the antibody and complement and bring the thing digested. Okay. Um

21:40 I think that was most of the . Any questions? So it's a

21:45 of a recap. Um All so here's the first process, I

21:52 you'd call it, we're gonna talk is inflammation. Okay. And there's

21:58 stepwise process to that. So, a look here. So what should

22:02 which will occur first and always occur inflammation, but there's one thing that's

22:07 gonna happen first and it's gonna trigger of the next steps. Okay.

22:46 timer going Alright, Count Down From : one. Yeah, it's sort

23:23 kind of release. It's gonna be that sets everything else in motion.

23:27 ? So let's see. Set of one. Any guess on number two

23:42 let her at me deep, it's deep. Then we get

23:51 let's see which one's next better before can exit. They have to stick

24:05 . There's no exit then that actually actually actually contributes contributes to the swelling

24:14 then we fix everything up repair that be like a scam or something like

24:19 . So we'll go through this. obviously a lot of cytokines are involved

24:25 inflammation. Okay, And, so we look at inflammation, we've all

24:31 this at some time or another. we have it right now, anybody

24:35 inflammation right now. Okay. The it could be fairly simple from,

24:43 know, you have a splinter in finger or something, or paper cut

24:46 , and maybe it's slightly affected. so now it hurts, right?

24:50 a red red blotch and it kind hurts. And maybe the warm to

24:53 touch, or it's all normal part the inflammation. So, so first

25:01 is meant to the response is meant contain the infection where it is

25:09 Right? So, again, we an example of a splinter,

25:12 Gets infected. So the inflammatory response meant to contain it right there in

25:17 spot. Another spread. Okay, . Is the main infection fighting cells

25:26 the beginning, are your neutrophils? . So neutrophils are circulating your

25:32 So, the infecting organisms aren't going be in the blood generally, they're

25:37 be somewhere in the surrounding tissue. , So that means you have to

25:41 the cells neutrophils out of the blood the surrounding tissue. So, a

25:47 part of information, is that is that to happen. Ok. Which

25:51 you're going to um make blood vessels in the area. So we get

25:57 local things, you're gonna make blood in that area more leaky more permeable

26:03 they can come out. Okay, that's what contributes to a number of

26:07 . The redness, you see the , the swelling that occurs because of

26:13 not only the red blood cells come , but other fluid blood comes out

26:17 well. That's what causes a swell uh it feels warm to touch

26:22 Often pains associated with it. So all these are all normal responses.

26:27 , so, of course, the step is, let's depend on the

26:31 of the damage, fix it, clot blood, Um, form a

26:36 perhaps these kind of things. now, um, the chronic,

26:42 talking this discussion is about acute the response, which means, you

26:49 it occurs over a period of 5 10 days. Okay, then,

26:52 done. Done. The chronic is it happens over and over again.

26:57 , chronic like very typical is intestinal . So, if you have food

27:03 , um uh, these can constantly cause inflammations in your, in your

27:09 and you get these this process it'll run over here over long periods

27:14 time, so that that can take toll on the body, of

27:18 Um but we're focused on the acute response here. So, among a

27:25 of cytokines are at least um because bringing together a number of different

27:31 You have to work on the blood to make them more permeable. You

27:35 them bigger generally as well. You to get various cell types to the

27:40 . So a lot of these things involved in doing that. Okay.

27:43 necrosis factors. One of those they that's damaged, we'll release this and

27:49 can be often be the first Okay. Something's not right here.

27:53 let's cause let's get information going. we need to take care of this

27:58 infection perhaps. Right? So the necrosis factor works in different parts of

28:04 body, especially in the liver. causes the liver to produce things called

28:08 phase proteins. Among these actually is um is one of those as well

28:14 some others. Um And so the is right as we look through this

28:20 dilation is the manipulation of blood Okay. To make them bigger

28:25 Dilate increased banker uh figure site So getting neutrophils out of the blood

28:34 the tissue to Vegas, Italians And then of course repair.

28:39 so a certain example and again this kind of the basic example with a

28:47 wound splinter or something. Where are on it that are affecting. So

28:54 call the subcutaneous um infection. Um so here's a section of the skin

29:00 see we're gonna involve different cell Okay, so again one histamine and

29:07 . Okay so histamine is one of that works on the blood vessel.

29:11 and what that means is we are to take a blood vessel in the

29:17 that initially looks like that. so this would be the this top

29:21 is the skin of the upper layer skin. Okay. Skin surface

29:27 Okay, and there's a blood vessel . Okay, so the action of

29:32 among others is to dilate it, gonna get bigger. So it gets

29:38 to the skin surface of the skin that's where you get the reddish kind

29:42 color comes from and that feels warm the touch. So what it also

29:48 is it will increase the volume of in that area. So remember,

29:53 this is local localized response. So blood vessels in that area. And

30:00 so think of a water hose, put your finger on top of the

30:07 , your resistance to flow, You're decreasing examiners, the water can

30:12 out. So if you make the bigger, if you could write,

30:17 be slowing down the flow of blood that area. Uh plus being

30:23 more blood volume in the air. . And so you need to slow

30:28 the area. Remember you're trying to out the fields that are coming through

30:35 you want to slow down there to them. So they'll begin to stick

30:40 the bus alone and squeeze out. , That's reasonable for, you

30:45 in the local area to increase blood by making it bigger and slow and

30:51 slow blood flow down. Okay? facilitate the exit of these neutrophils.

30:57 . And so kind and self also of the process is to um take

31:03 cells that make up the bulk Okay. And kind of pry them

31:09 . Okay. Because remember that's you make space between the cells so you

31:13 pop out. Okay. And so what kinds do okay um you have

31:20 local trains and things that kind of to the same process because there's not

31:25 history but the other chemicals also act what we call vaso dilation factors.

31:30 what we're talking about. We're making big right up up here is vaso

31:35 history. Can do that as well other side. Okay. And so

31:42 prostate glands. Okay, so uh here are here, right, this

31:49 damaged isn't damaged cells in the area that can trigger the release of the

31:53 necrosis factor with them. You can getting the blood travel to your liver

31:59 cause the formation of these other specific . But also you may have macrophages

32:05 floating around here that can that combined these right the champs and that can

32:09 set a kind production as well. so that all to get cells to

32:15 site to these histamines, et And so I'm not sure your animation

32:20 this as well. Um So project though are released and these were my

32:28 and engineering because you wanted to be to that something's happened to you write

32:33 , you know that, oh, have an infection. I need to

32:35 this room where it's alert you to . There was something going on

32:39 Okay, then what happens is um, these uh, this

32:49 so not myself. But but what is, let's just show the picture

32:54 . Okay, so here is the vessel in the area. So they

33:00 have dilation. They were gonna kind pull the cells that make up the

33:05 a little bit so they can squeeze . As you see, this neutral

33:09 is rolling down along the side of vessel. There's actually uh uh,

33:16 of needs to help promote the release these cell surface molecules that kind of

33:23 like velcro to kind of stop the to slow them down. Those are

33:27 along. Okay. And then then other side of kind of kind of

33:33 apart the cells of the blood vessels that's how they squeeze through. So

33:38 , the uh, squeezing through is Diet Pegasus. Okay, the kind

33:44 slowing down while they stick to the surface before them is the margin

33:48 margin Nation is kind of they stick the wall and they squeeze out.

33:53 the diabetes is okay. Um, , so initially it's so, so

34:00 the neutrophils exit, right, exit blood vessel. Of course, you're

34:04 have other food comes with a filter only only come out other stuff with

34:10 what contributes to the swell. And then of course they're they're fighting

34:16 . You have so after a while have looking forms pus. And plus

34:22 basically uh your white blood cells, of which are still alive from the

34:28 dead cells. And so it's kind collection of all that stuff.

34:33 Um and then then that's followed by . You may have some depending on

34:40 severity of the injury. You may some lack of movement, maybe somehow

34:45 movements impaired in the area or otherwise impaired until prepare occurs and repaired.

34:52 is basically uh can be uh cell to replace. That sells blood scab

35:00 , these kind of things. And that leads to a what you see

35:04 here which can eventually gets it clears and back to normal. So let's

35:12 let's show this animation. Uh Come one in a second. Uh Let's

35:20 here. Okay top. There we . So here is that's gonna be

35:32 same splintered kind of example here. you get your capillaries in the area

35:38 . Super tiny one cell thick red cells and mixed in with you see

35:45 hills there are the white blood So here's macrovision, Here's the subcutaneous

35:52 pathogens. Here comes macrophages in the . Remember your fixed macrophages,

35:57 These these may be sitting here just out uh you have released a set

36:02 contracts. That's the pants T. . R. Effect. Right?

36:06 among the cited content will be histamines etcetera that will blow that area.

36:13 here's cells that make up the blood . Okay. And video cell then

36:19 have these uh white blood cells will all cells have these kind of glycoprotein

36:25 on the surface and some things are to here's how it slows it

36:29 That's rolling along. All right. then uh you have to break apart

36:36 connections. Right? So don't worry the name here. Uh these are

36:41 molecules and they interact with blood cells that I can to kind of help

36:47 kind of analogous to velcro sticking sticking those cells. And then we have

36:56 effect of Yeah that helps break apart connections between these cells temporarily at least

37:04 that they can slip through. So sticking part is kind of the margin

37:10 that what you just saw is a or squeezes through. Okay, so

37:14 they can get into the surrounding tissue they can do their thing ties.

37:21 and then of course uh for sales out. And so you have more

37:27 kind of more history to kind of the dilation effect than the and the

37:33 they have mass cells in the area also triggered to use this to me

37:36 all to work on the blood vessel dilation. It's like when you see

37:40 background kind of fill up that's a . So it's growing up in the

37:45 . Um, and so the but again, this is classic profit

37:52 . They work on the to heighten sense of pain in the area.

37:57 so you get your basic sign Warm, pain, swelling.

38:04 so, uh, inflammatory response. , acute inflammatory response. Right?

38:15 , so, uh, any questions that? So, um, when

38:23 , this can be an issue bad you? Okay. Is if you

38:29 , so we talked about endo toxin gram negative infections. So it's a

38:35 materials release the material cause shock. , it's when you have a,

38:42 think that's an inflammatory response that's not just it looks like the area

38:46 the body wide. Right? So you have a very negative infection in

38:49 blood, right then potentially all the and much more cells in the body

38:55 respond to this thing rather than just a local effect. Right? And

38:59 , you know, the effects of response dilating blood vessels, right?

39:04 that happens in the body wide Now you have blood vessels that are

39:07 be, you know, being dilated included coming out every blood volume will

39:13 down as a result because it's happening wide, not just locally. And

39:18 when you're going to shot. And you're using blood volume from numerous blood

39:23 in your body and blood pressure goes , um, etcetera. So not

39:29 think so. So a body wide response is something that's very dangerous if

39:33 happens. Okay um And then the is one of those that can cause

39:40 um Okay uh fever. So fever again something we've all experienced. Um

39:52 it's really just a resetting of a resetting of the body's thermostat. Okay

40:01 hypothalamus is what controls your body And the thing that will adjust the

40:12 set point. So normally your set is at around 37 38 or so

40:20 Jeremiah's half of the year. So we're always a little bit different but

40:26 within that range. The and so happens is something triggers it to to

40:35 . Okay so pira genes are those that cause beaver. Okay you can

40:41 what's called endogenous or exogenous pira Okay so outside the body and things

40:47 bacteria, viruses, pathogens that come your body. Then they trigger end

40:52 endogenous pirate. So chemicals you produce introducing one. Uh I 01 please

40:59 directly on the hypothalamus. Okay and the set point uh Up. And

41:07 So a psycho typical cycle if we 37 c. as the set

41:13 Okay Um the presence of Pira Jin's . Oh like that. Okay so

41:20 we go up to say 40 give take we shift to a higher set

41:26 . Okay. So much like if cold and you go in the house

41:33 you turn the thermostat up. Okay Are you going to immediately be

41:42 You're gonna feel cool for a while you're until that temperature gets to tell

41:49 house temperature gets what you said. that right? So let me

41:52 So the same in your body. not instantaneous. So you turn the

41:56 up in your body. It takes bit for your body to catch up

42:01 that new set point. And so you do you're gonna feel chilled

42:07 Um Typically what happens is you kind oscillate between chills and sweats chills and

42:14 because that that set points kind of up. Okay so you kind of

42:22 the effects of that as it goes . Your body is not your bodies

42:26 this higher set point but it goes a little bit and it takes a

42:30 to readjust. You're gonna feel hot you get to that point. So

42:34 why you kind of go through oscillating and low Children chosen the and sweat

42:42 finally you you overcome the infection fewer and you go down to your whole

42:49 point. Okay? Um Now you even even though you have your uh

42:58 point has increased and your body catches with that temperature you still don't feel

43:03 obviously. Um But it is serving purpose. Okay so the most obvious

43:09 probably you know pathogens that affect our Bacterial pathogens um you grow them at

43:17 in the lab. Right? So your body type, that's what they're

43:20 to. So if you elevate that will affect their their growth. Okay

43:25 it does that but probably more importantly helps your immune system. Okay.

43:32 uh increases T cell activity. So of the things about your adaptive immune

43:37 , B cells and T cells they time. Okay so they have to

43:46 engine, they have to respond to and that's there's a time element to

43:51 . Okay. And so wherever you buy time to help them out that's

43:58 your favor. And so slowing down growth is one of the ways so

44:03 slows them down T cells and B to find them and recognize the engine

44:09 then do their thing. Okay so cells as well learn um a particular

44:15 cell type is very it's kind of master of the whole thing right?

44:20 the B cells that need activated by cells and B cells make antibodies and

44:25 cells kind of deal with intracellular So but the whole system is kind

44:30 regulated by certain T cell types and increase their activity to do this during

44:36 . Okay and then iron uh again really goes back to thinking about growth

44:42 ? And what's needed for growth. . Iron turns out to be a

44:46 essential elements for pathogens. Okay for life but I mean you kind of

44:52 with them over over the credibility of right? You many different ways certainly

45:00 hemoglobin and hemoglobin binding option is a source of iron but also other types

45:07 well. So you have a definite for it and you need to hold

45:10 to it. So if you keep away from pathogens that infect their girls

45:14 well. So um so it does definitely has a role in your innate

45:24 system to slow down the growth and mobilize your adaptive immune system Check um

45:32 are too high attempt to high attempt not that is detrimental. Okay because

45:37 body can't sustain that but something that's one a 11 or two, you

45:41 that's sustainable but but not when you 104 105 that's not your body can't

45:47 very well like that. We need do something about that. But most

45:53 us that go through the typical you know it's one that uses

45:57 one of 112 is typical. OK so compliment so compliment um is our

46:12 factors that are not compliment or not cell type. Okay. They're simply

46:17 proteins that are floating around your Okay. And unless until your until

46:24 have an infection, compliment is in inactive form. Okay so there's ways

46:31 activate complement to make it do its . Okay and there's three ways that

46:38 be triggered. Now there are a of proteins that make up competent.

46:43 uh but it really boils down to the C. Three and C.

46:51 . Those when those can activate it when most of the action occurs,

46:56 compliment. Okay so again there's like of these things that are inactive and

47:03 like a cascade effect. So for C. Three you see there is

47:09 , it's activated by I think Two. It is formed C.

47:13 A. And B. Okay Then activates five right into C.

47:19 A. And B. And it of goes keeps going so C.

47:22 and activated seven and 89. So that's a cascade but it's when these

47:29 activated like I said that's when most the work occurs. Okay so um

47:37 you have certain cell types that work the adaptive immune system. Macrophages,

47:42 cells compliment also work with the So remember uh complement the classical

47:51 This is the first one. Okay simply binding to uh antibodies activated.

48:01 everybody's bound here. Okay and there's competent factor. And so anybody buying

48:08 a pathogen that activates the anybody's Now the effects of senior.

48:15 optimization site A'Lexus inflammation those three outcomes the conference activated are the same but

48:24 power is activated, those are the actors. Okay so anybody is one

48:29 to activate um another way is to to uh cell surface black. Oh

48:38 bacteria um have these or other Okay and compliment can combine these.

48:48 . And that in itself can trigger activation. Okay. Um and then

48:54 is collected. Okay so elections are of those uh mentioned earlier tumor necrosis

49:05 can go deliver and that contribute to to produce one of these c reactive

49:11 . And and uh election is one those. Okay, so elected by

49:18 very common manos and other types of are commonly found on bacterial surfaces.

49:26 , so like that's what they Okay. And so that they can

49:32 complement activation. Okay. So um so again the outcomes you see the

49:38 outcomes here optimizations that causes inflammation. it's the same, the same three

49:43 occur regards of how it's activated. . So what are these what we

49:47 the optimizations? Okay that's the it's like antibody can be so and then

49:56 it can take up specific cells. take it up. Okay um cytology

50:04 so this you see here complement proteins together to form these little channels in

50:12 cell membrane. Okay basically the stuff out of the cell killing it.

50:17 what they call a membrane attack complex have these complement proteins. Um This

50:24 more effective with graham uh negatives. because gram positive never have a liking

50:34 wall covering. Okay and so we don't really fit into a cell wall

50:40 fit into a memory. So remember negative having outer membrane layer. That's

50:44 they're more susceptible to this kind of . Okay and then uh finally is

50:52 inflammatory response so concrete can um bind cells involved in inflammatory response for this

51:01 . Histamine. So kind of enhance uh for a response by producing these

51:07 the formulation of these cytokines. Okay again all three of these are our

51:14 of activity no matter how it's Okay um and then uh let's see

51:24 . So interference. I think we about that in But their defense against

51:31 , antiviral defense and so we have classes. Type one is the one

51:38 anti bar. Okay and so how works is like this. Okay so

51:45 have a virus infected cell. And you have um that infection itself

51:55 what triggers the formation of interference. . Design defects and triggers that and

52:07 any neighboring cells. Okay so in nearby nearby will if they have the

52:15 for it will buy interference. Okay those cells take it up and that

52:20 as a activator to produce viral antiviral . Okay so again these are cells

52:29 the vicinity of those infected self. and um and the net result is

52:37 viral infection basically stops because these these cells have these antiviral proteins that the

52:44 comes in. They basically block the . Okay so again the cell that

52:51 affected is gonna like this a common but the neighboring cells and and protected

52:57 uh by the action of interference that take in. Okay so this was

53:07 I think. Um it was like of the first biotechnology products that mask

53:12 they appear on the antiviral drug. it didn't prove to be successful because

53:19 the toxicity of it. So in doses it's toxic and it's not long

53:25 but it is still effective um in you go to the hospital and your

53:31 infection they do give you a shot because it is effective in kind of

53:38 in that setting more local infection kind way in a uh in in administering

53:44 uh in small doses that works. effective but not as a marketing as

53:49 pill for mass consumption doesn't that doesn't work. Okay. Nonetheless it's it's

53:55 is effective in its control. Um The other type of interfering is

54:03 that activates neutrophils and macrophages. Okay what that means to activate the macrophages

54:11 neutrophils all is it may initially look remember the key is that um it

54:19 look like this initially. Okay when activated it will have the formation of

54:30 super parts. So that's an activated for example. Okay. Creating a

54:42 pods and how it helps bind the and take things in. Okay.

54:47 create more of those it's really through action of it acting that actually causes

54:53 But nevertheless that when you activate it there's different ways to activate you can

54:56 with interferon, you can do it certain t cells that result the

55:01 You create more of these super pods that enhances Vegas halitosis. Okay.

55:09 so the uh antimicrobial substances. Okay this is the last um so these

55:26 take different forms. Okay so iron proteins to remember that iron is a

55:30 thing in terms of keeping away from to slow their growth down. So

55:34 have things like transforms uh bind iron in fact but in actuality pathogens also

55:43 their kind of iron binding protein. what scenario for by specifically binding um

55:54 antimicrobial peptides. These are widespread uh cells in our bodies can produce

56:00 Okay. They kind of act like uh form a tunnel in the assembly

56:08 the tunnel in the membrane causing license of like the membrane attack complex we

56:13 talked about this will be the same of site. It's really widespread in

56:18 of what it can attack. Not just bacteria but different types of

56:24 um and founding like macrophages uh it other other cell types in the tissues

56:32 the body. So there's something like or 60 no more than that.

56:36 like hundreds of different varieties of these um that have this antimicrobial activity.

56:43 . Um so is uh recap this and talk a little bit about adaptive

56:53 but any questions about response amps, have you? Okay, so let's

57:03 at this question here. Just kind talked about I think all these things

57:09 . Okay, so which choice is ? Transference, remembering attack complex and

57:19 type one compliment. You will try again. Okay. All right,

58:22 down from 15 321. All So it is a choice. The

58:45 is Um a is true. Okay the true one. Um Remember the

58:53 complex, is that accurate compliment forms um It's a compliment. Can't figure

59:01 anything. It's a protein. Okay interfere on type one. That's the

59:09 amps. Are these antimicrobial peptides transfers iron binding chemicals? Um Okay so

59:20 are a a book uh and of in electrolytes have kind of a summary

59:27 here's the physical and chemical factors if like to Use that. There's also

59:33 of 2nd line defense. Um You the the backward quiz this week.

59:41 you good uh sampling the kind of . You'll see the same ones you've

59:46 seeing clicker questions. So um so talk a little bit. This doesn't

59:54 about the system. We'll get more the details about it next time but

59:59 for now kind of setting it So is your third line defense is

60:05 termed and above T cells B cells also remember that macro failures interact.

60:14 macrophages aren't technically part of this this but they interact with these cell types

60:23 dendritic cells. Okay so uh interact T cells. Okay. Um so

60:38 there's kind of an overview so we we distinguish these two systems by huber

60:43 system which is your B cells and and their cell mediated community.

60:49 Um and each have their roles and uh there of course are different types

60:55 lipid science, B. B. and T type lymphocytes um T cells

61:03 of mature in the they both made both but they traveled to the diamonds

61:07 T cells travel to the finance really uh B cells in uh panic

61:14 Um But in terms of their what do. Alright. So b cells

61:21 they differentiate into what's called a plasma and plasma cells. What makes the

61:25 ? Okay. Memory cells remember there's is actually memory to both. Your

61:31 . Doesn't really go into it but not gonna expected to know it but

61:36 actually memory cells that are also part the T cells. Both sides have

61:40 memory component. Okay I'm most familiar the b cells that have memory component

61:47 . You get vaccinated if the if get affected by the same and then

61:53 you will produce antibodies. That's the memory component. Okay but there are

61:59 b cells that that's what they Right? So memory cells don't produce

62:04 but plasma cells do Okay. And the end the role B cells deal

62:11 extra psychopath. Okay so antibody cannot inside of a cell and attack

62:19 Only combined to pathogens that are outside . Okay so um the tea's types

62:28 cell types they're what are called defector . And these deal with the interests

62:33 the path. So they recognize cells infected and they deal with that.

62:40 your site. A topic T Okay. Um Used to be called

62:45 a type called explanatory T cells. just typically called T. Helper cells

62:51 . Um The other cell types of . Helper cells and other types there's

62:57 two types of T. Helper cells one type activates um B cells.

63:05 another type activates Macrophages and dendritic Okay so you have a differentiation between

63:15 2? Okay. Um and then cells. Okay so we'll see how

63:24 cell works is by being activated. not always but usually activated by a

63:28 type of T cells. T. cell to produce antibodies and then macro

63:32 and uh work with other T. cells to activate them. Okay um

63:40 so the so antigens antibodies. Okay is typically going to be uh it's

63:51 course what what binds to anybody. and so these are gonna be various

63:56 of typically protein in nature but they be lots of different chemical components.

64:02 lipids can be antigens um you know what's on the periphery of the

64:08 right, proteins that can be like , all can potentially be antigens.

64:15 , so that's the thing about the system. It is only stimulated by

64:21 presence of managing so it must be scene and then bound to it and

64:28 stuff happens. Okay. So uh in terms of the antibody, there's

64:35 of two ways to look at One is the epic Tope. So

64:40 epa Tope is the specific part of engine that is bound. Okay,

64:46 as an example here, this would gray. Big gray blog is the

64:52 . Okay, that's what's recognized in um And again, is the actual

65:00 . Okay, that's where the actual occurs. So antibody or anti gen

65:08 it is an epic Tope where the actually occurs. Okay. And so

65:13 there's a there's a as we'll see we don't go into the details because

65:18 very the immune response involving the death the system is very complicated.

65:23 And there's memory to it. There's a learning curve to it. So

65:29 cells that are formed initially in response an uh actually get better at bonding

65:36 action, as long as we keep exposed to it. Okay, so

65:41 self formed aren't isn't as strong in of their immune response, it gets

65:46 . So there's also a learning curve goes with it. So um of

65:50 it's all involved chemicals getting activated, like that, but we're not gonna

65:56 into complex nature of it, but of more overview. But uh I

66:03 the point I'm saying it's more complicated it is to hear, but,

66:07 know, this is this this level just fine, right? This will

66:11 what you need to know. Um but proteins tend to be the

66:17 engines in terms of there, there's large variety of if the number of

66:23 that tends to be a type, energy is buying tightly to.

66:27 less so with carbohydrates and fats, not the same variety of those types

66:34 there are proteins um and so determines means the same thing.

66:43 so um, Let's see any any , any questions. We'll go ahead

66:51 stop there and pick up with finishing 17 next time,

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