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00:10 Mhm. Hey, oops. Um get started here. He um,

00:30 see. So I sent out an um, yesterday, basically tell you

00:37 you do. So we got the quiz again this week, mastering next

00:43 . Uh Let's see, what else gonna finish up 16 today. Um

00:48 the second part of the in eight system, Thursday is the adaptive immune

00:54 and we'll do a bunch of uh questions around that discussion. We'll

00:58 we'll start with the very beginning of 17 at the end today. This

01:03 kind of what you um the uh . So remember the Sky Group opens

01:11 Friday. Ok. So we can a spot. Um, the exams

01:17 , uh still a couple of weeks , two plus weeks away.

01:21 um, certainly if you have questions , you know, material,

01:26 let me know combining office hours, . What have you? Ok.

01:32 Then, uh let's see, next we'll finish up, um, eat

01:38 three and start, you know, the following week. Ok. Um

01:44 we may, may start some of here depending on, you know,

01:51 , I'm thinking that we only have come. So, class ends on

01:55 , December 1st. I think We may not have to have class

01:59 day if we keep on schedule. , uh, anyway, um,

02:07 , oh, the other thing was grade. So I have calculated that

02:12 be posted in the morning. I'm just about that but it'll be

02:16 in the morning. So, I didn't do all the heavy lifting

02:20 would do if it was a final , but it's good. It's,

02:22 a fairly close estimate. Ok. I didn't go through and so like

02:29 , like the, um, forget top, the top something, clicker

02:34 or whatever a game. I didn't all that, but it's still,

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

02:41 uh it also includes the extra credit the, I assume I was gonna

02:46 out the survey. I have to until you get extra credit for

02:49 So that's figured in uh the isn't figured in, but you can

02:53 just add a point or something to grade. So anyway, it will

02:56 a close up for you now and , and the, you can look

03:00 , I'll put it in the, email ahead of time where I post

03:04 . Um But it just captured it really like exactly what it's written

03:08 the sys, right? Just taking point on black board and just following

03:12 1234. OK. Um And uh was the other thing? The uh

03:20 um I can't remember but uh um the scale. So it's a numerical

03:30 obviously. And so you're gonna compare number to the scale that's in the

03:34 on, on the, we talked the grade and stuff. I also

03:38 to that scale in the email as . So that's what you're gonna compare

03:41 two to get a Testament of your grade. Ok. Um All

03:47 So, yeah, so watch out that and like I said, I'll

03:49 an email out because of that, , in the morning. So,

03:54 , let's see. So, I don't think the drop eight is

03:57 16th. Is that right? I the 16th don't hold me to

04:01 but, uh, I just wanna you that information to make a decision

04:06 you are, if you're thinking about . Ok. Um, and so

04:11 can easily figure out because the question becomes, what do I need to

04:15 on exam? Three and four, , blah, blah, blah,

04:18 ? So you can do that you just plug in the plug in

04:21 right? And that will give you least the upper upper range,

04:25 So that's easy to do and just the steps that are in the,

04:30 , that are in the exam, mean, in the. So,

04:33 , so, uh, the, , ok, if you have questions

04:38 let me know. So let's, , so we're gonna do, we'll

04:43 with two questions and then uh a bit of a, it's a recap

04:50 last time. OK. So let's here. So we talked about all

04:56 these last time. Ok. uh take a look, um,

05:04 is the true statement. OK. it's not 80 D obviously, it's

05:12 F yes. And on, on , on F there, you're not

05:49 see that on an exam, You have to identify visually what cell

05:53 , but I just threw it in grins. OK. Cut them

06:30 You. All right. Coming down six buy for your, it's gonna

06:52 Yes, it is. C uh basophils, the primary foci excel type

06:59 neutrophils initially, then followed up by um to like receptors. They don't

07:07 anything, right? They're not a , they're a surface molecule that binds

07:13 a pamp, right? And that cytokine release and the alarm bell.

07:18 like receptors are the alarm system, to speak. Uh pamp is

07:23 Um That's what that is the um um that's involved in think of that

07:31 facilitated pags. So it's when it PAP is coated with antibodies are complemented

07:38 that's taken in and it's for cells pathogens that aren't easily fis OKS are

07:45 to them and C molecules. So , that's your, your barcode on

07:50 cell and tissues. It's your self . OK. So we'll clarify that

07:55 here in a second, just as recap uh leptos. These are actually

08:00 uh neutrophils. They have that weird um nucleus. OK. So those

08:08 blobs are uh it's DNA are Um But again, I'm not

08:15 I just do this in just for . It's not, you're not gonna

08:18 images where you have to identify the type based on just the image.

08:23 don't worry about that, but uh a nursing kill, you have to

08:27 that, but not here. Um . One more question before we do

08:32 content here. So which virus infected might be dealt with by. So

08:38 remember the extracellular pathos, intracellular pathos systems systems to deal with that,

09:12 . OK. OK. Put the on. OK. Counting down six

09:52 that it is going to be natural cells. OK. So those and

10:01 up we haven't really now I talked little bit about it but uh certain

10:08 cell types uh what are called cytotoxic cells. Uh but them and natural

10:15 cells deal with infected cells. Um OK. So a little bit

10:20 a recap here. So innate So that's what we're doing talking about

10:24 16, right? So think about . 1st and 2nd line defenses,

10:28 line physical chemical barriers to remember your barriers like your skin because membranes also

10:35 secretions and those serve as chemical They can take lysozyme is very

10:41 Um The simply the the nature of secretion or maybe salt to your city

10:48 , that it can be a Um second line defense. But also

10:53 the first line I remember is is microbiota. So that also is part

10:58 second line are typically cell types Um So inflammation we'll talk about

11:05 Uh fever, these are processes of , can involve cell types for

11:10 Um But uh no specific cells uh like they use of or release toxins

11:19 things like that. So various types um um defenses to, to counteract

11:26 pathogens. And so we talked in question about PMS, right? So

11:31 are, these are the peripheral features pats, uh outer membrane. So

11:39 flagellum. So things on the external of this um pathogen. OK.

11:46 to the sector combined. Uh and effect is to cause these of cytokines

11:51 these are gonna alert cells, they're bring cells to cy of infection.

11:55 can uh have varied effects. Um uh The uh we'll talk a

12:02 about cytokines today in the context of response. There's a lot of those

12:07 here in the inflammatory response to, do different things. OK. Um

12:14 there's uh OK. These are the types. We went through these

12:19 Uh each have different roles and basal are mostly um kind of releasing release

12:24 different types of chemicals and cytokines. involving the inflammation and other processes.

12:32 and figures at times. But their is also toxin producers. But to

12:36 uh to really deal with large monocytes differentiate the macrophages uh in lymphatic

12:44 . So, lymphatic system is about pro protecting against inhaled ingested microbes.

12:51 your tissue can be quite dense in parts of your body and these are

12:57 of macrophages, uh B cells, cells to, to help fight

13:02 Um And then uh let's see what ? Oh Here. So then uh

13:09 aosis oxidization, right? So we'll about these today. We haven't gotten

13:13 yet but uh just quickly on the C. So this is important because

13:20 your ability to recognize something has an that shouldn't be in your body can

13:28 occur if your body knows and differentiate what's yours and what shouldn't be

13:37 And of course, it occurs through occurs through biology occurs through molecules of

13:41 type. And so self antigens are of like your barcode to identify yourselves

13:47 your own. OK. So if comes in that doesn't have that same

13:50 code and that's a trigger. And that's what can um uh alert

13:56 immune system cause different effects. So have that system is broken down into

14:04 types depending on the subtype. So I always do two first because

14:10 the easiest, it only has three , right? It has B cells

14:14 and dendritic cells. So the cell that are called antigen antigen presenting

14:19 they show antigens to the body. . That can then respond different

14:25 respond to them. Uh So everything that's not in that group is am

14:31 one is basically all your body Ok. Uh Not red blood

14:36 they have their own system. That's A bo system, their system.

14:41 ? But everything else that's not a two is a type one.

14:45 And so, um and so we'll , as we get into the adaptive

14:50 system, you have certain of those interact with these types of C

14:57 others interact with these. OK. that's what kind of differentiates their function

15:03 talking about different types of T cells with these two. In fact.

15:09 it, it'll, you know, keep repeating this and it will become

15:12 as we go through. Um but then we see engines uh here

15:16 just on the surface of the they originate inside the cell. Of

15:20 , they can, then they can we can see molecules inside that are

15:26 and they combined a viral piece, ? That's a piece of a virus

15:35 of uh another bacterium. Sometimes bacteria enter into the cell and, and

15:43 out. So maybe it's a piece that and it goes to the

15:46 right? And now the immune system detect a G is for an

15:53 can detect. Oh, here, it goes to the surface and now

15:57 shown to the body, well, inside, it's invisible, but once

16:00 gets in the outside then other immune cells can respond. A T cell

16:04 respond or what have you. And that's how you can find out

16:09 going on in terms of your immune . Uh, or you can have

16:13 like this. Right? And um, you know, infected

16:18 cancer cells can have different appearances on surface. OK? Maybe they lack

16:24 C molecules altogether. That's what natural cells look for. So they,

16:29 that tells the body, it's, not normal, it's abnormal not to

16:32 MH CS on your surface. So infections like a viral infection, not

16:38 but some can cause these changes to surface. Certain cancers, certain cancers

16:43 do that. And so that's what metro curro cell looks for. Uh

16:48 another type, don't worry about Now, what, what's called the

16:54 T cell? OK. These two for uh um uh infected cells are

17:01 showing antigen, OK, through their C one mole. And that's the

17:09 there. And so it, it varies and an affected. So

17:15 depending on the viral type and it will um have different responses.

17:21 may be like this where a lax now cytotoxic natural killer cell may be

17:25 the lookout for it or maybe it have that response and it, and

17:29 does have MH C ANS on but they show a, a part

17:35 that infecting organism as in on the . So you have cyto toxic T

17:41 , I can recognize that we'll talk that in 17. But this over

17:45 worth mentioning. So the point is got multiple ways to deal with different

17:50 of infections. OK. But there a, so this is a,

17:54 an intra 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 I need coli here foodborne illness, right? So

18:22 have both, obviously, both can you and we have ways to deal

18:25 those. And we do, we specialized cells that can deal with each

18:29 . OK? So you do have lot of defenses. I mean,

18:34 mentioned what I did earlier, the chemical bears etcetera. So we got

18:37 lot of stuff going on that can happens. Uh it's gonna happen that

18:41 be triggered in the course of an . OK. Which is all good

18:45 you. Um Any questions about So engines OK. Um OK.

18:53 then lastly ptosis optimization. Uh so remember, you know a a

19:00 macrophage uh as part of the process also have. So this is a

19:06 of tiny writing but that's a total receptor TLR for short, right?

19:10 so that can the macrophage can not engulf and ingest and break it

19:17 but in the binding part, it , you know, have a tool

19:21 receptor and cines to alert more cell um these uh once it gets crunched

19:29 , right? So this is the zone, then fuses with a Lysa

19:33 , right? And so then it digested, that material can exit.

19:38 , but also we have, this have MH C molecules, OK.

19:43 A macrophage, if that's what it , would be a type two.

19:47 . And so it will bind to of these particles. OK, then

19:52 it c two antigen and then this be um, the, a part

20:03 a virus or whatever crunched up in and show it to the body and

20:08 it's visible to the cells of the system. OK? That's what

20:13 that's what the antigen presenting cell OK? Shows whatever digested to the

20:19 . So the immune system can respond needed. May, maybe it's

20:22 maybe it's, if there's no response it's not, not a threat,

20:25 maybe it is. So that's, to be determined by the cells that

20:30 with it. OK. And then is the ization. All right,

20:35 have the pathogen here and it's coated these little yy shaped thingies or

20:44 OK. So, antibodies by antigen that's what it's doing. And so

20:49 have these, these parts of the bind to the pathogen, right.

20:59 part combined to a cell like a to different body parts. And so

21:09 so optimization accounts for those pathogens that easily fit because they're slippery like a

21:16 a thick capsule or something. So have antibodies to it or complement is

21:21 other one. So are both s complement and antibodies coat the cell that

21:27 it easier to bring in the The fig cytic cell can bind to

21:32 antibody or complement and bring the whole and digest it up. OK?

21:39 OK. I think that was most the stuff. Any questions?

21:44 So a little bit of a Um All right. So here's so

21:51 first process I guess you'd call it gonna talk about is uh inflammation.

21:57 ? And there is a stepwise process that. So take a look

22:01 So what should be, it's really first and all these occur in

22:06 But there's one thing, it's really happen first and it's gonna trigger each

22:11 the next steps. OK? The are going, all right. Count

23:15 from 321. Yeah, it's set kind of release is gonna be first

23:25 sets everything else in motion, So let's see. Set of kind

23:30 is one, any guests on number or let her at me d that

23:46 , yep, it's deep. Then get mm Let's see which one is

23:56 better before they can exit. They to stick. All right, give

24:04 three. They're not exit. Then actually the egg actually contributes, contributes

24:12 the swelling and then we fix everything , repair. It could be like

24:17 scab or something like that. So, uh so we'll go through

24:22 . So obviously, um a lot cytokines are involved in inflammation.

24:27 And so as we look at um we've all had this at some

24:33 or other, maybe we have it now. We have inflammation right

24:37 ok. Um The um, it be fairly simple from, you

24:43 you had a splinter in your finger something or a paper cut maybe and

24:47 slightly infected. And so now it , right? Makes a red,

24:51 blotch and it kind of hurts and the warm to the touch or is

24:54 normal part of the inflammation. So, um, so first inflammation

25:02 meant to the response is meant to the infection where it is encountered,

25:09 ? So, again, if we the example of a splinter,

25:12 it gets infected. So the inflammatory is meant to contain it right there

25:17 that spot that it spread. Two is the um the main infection

25:26 cells in the beginning are your right? So, neutrophils are circulating

25:31 your blood. So the the infecting aren't gonna be in the blood.

25:37 , they're gonna be somewhere in the tissue. Ok. So that means

25:41 have to get the cells neutrophils out the blood into the surrounding tissue.

25:47 , a big part of inflammation is is getting that to happen.

25:51 Which means you're going to um make vessels more in the area. So

25:57 , it's a local thing, you're make blood vessels in that area more

26:01 , more permeable, so they can out, ok? So that's what

26:05 to a number of things the redness see in your inflammation, the the

26:12 that occurs because of course, not does red blood cells come out but

26:16 fluid of the blood comes down as . That's why it causes the swelling

26:20 uh it feels warm to touch, , often pains associated with it.

26:24 these all these are all normal Ok? So, of course,

26:29 last step is let's depending on the of the damage, fix it right

26:34 blood um to form a scab perhaps kind of things. Ok.

26:40 um the chronic, we're talking this is about a acute, the acute

26:47 response which means, you know, occurs over a period of 5 to

26:51 days. Ok. Then you're done there. Chronic is when it

26:55 over and over again. Ok. like a very typical is intestinal

27:02 So, if you have food um uh these can constantly be triggered

27:07 inflammations in your, in, in gut and you get these, this

27:12 occurred over and over again, over periods of time. So, uh

27:15 , that can take its toll on body, of course. Um But

27:19 focused on the acute observatory response So, uh among the, a

27:25 of cytokines are at least, um you're bringing together a number of different

27:31 , you have to work on the vessels to make them more permeable.

27:35 make them bigger generally as well. have to get various cell types to

27:39 site. So a lot of these are involved in doing that.

27:43 The tinary process factor is one of a cell that's damaged will release this

27:48 that can be often be the first of. OK. Uh Something's not

27:53 here. Let's let's cause let's get going. So we can take care

27:56 this potential infection perhaps, right? the uh in two necrosis factor works

28:03 different parts of the body, especially the liver and it causes liver to

28:07 things that are called acute phase Among these actually is compliment. Um

28:13 one of those as well as some . Um And so the stages,

28:18 , as we look through this vasodilation the manipulation of blood vessels.

28:24 To make them bigger, actually dilate bang uh py migration. So getting

28:32 out of the bug into the tissue fatties pathogens and then of course

28:39 Ok. So um sure example, again, this is kind of the

28:45 example of a uh a puncture a splinter or something where uh there's

28:51 on it that are infecting. So call subcutaneous um infection. Um And

28:59 here's a section of the skin, see, and we're gonna involve different

29:03 types. OK. So again, one of histamine and kinds,

29:07 So histamine is one of those that on the blood vessel. OK?

29:12 what that means is we are going take a blood vessel in the area

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

29:21 is the skin, the upper layer skin, ok. Skin surface

29:28 Ok. And there's a blood vessel . Ok. So the action of

29:32 among others used to dilate it, gonna make it bigger, right?

29:38 it gets closer to the skin surface the skin. And that's where you

29:41 the reddish kind of color comes from it feels warm to the touch,

29:45 ? And so what it also does it will increase the volume of blood

29:51 that area. So, remember remember is local, localized response,

29:56 So with blood vessels in that area will die. And then, so

30:01 of uh a water hose and you your finger on top of the

30:07 your, your resist resistance to right? You're, you're decreasing G

30:11 if the water can come out. if you make the hose bigger if

30:15 could, right, you'd be slowing the flow of blood in that

30:21 Uh, plus being bigger, more volume in the air. Ok.

30:26 so, uh, and you need slow down the blood flow in the

30:30 because remember you're trying to pluck out neutrophils that are coming through, so

30:35 wanna slow down, they make them they'll begin to, uh, stick

30:40 the blood vessel wall and squeeze OK. So that's reasonable for,

30:45 , you know, in the local to, to increase blood flow by

30:49 it bigger and slow and consequently slow flow down. OK? To facilitate

30:54 exit of these neutrophils. OK? so uh kind itself also part of

30:59 process is to um take the cells make up the blood vessel,

31:07 And kind of pry them apart. ? Because remember that's you gotta mix

31:12 between the cells so you first can out, ok? And so that's

31:16 kinds do, OK? Um You other leo trying and things that kind

31:22 contribute to the same process because there's just histamine, but the other chemicals

31:26 act as what we call vasodilation That's what we're talking about and we're

31:31 it big right up here is His toy can do that as well

31:37 other, other side. OK. so um prostate glands. Ok.

31:45 , uh so here up here, foot actually damaged, physically damaged cells

31:50 the area and that can trigger release that tumor necrosis factor. Then it

31:56 travel, getting the blood travel to liver and then cause uh formation of

32:01 other specific proteins. But also you have macrophages just floating around here that

32:07 , that can bind to these right PMS and that can elicit cytokine production

32:11 well. And so that all all get cells to the site uh to

32:16 histamines, et cetera. And so not sure you animation show this as

32:21 . Um So prostate madness though uh , are, are are released and

32:28 were my nerve end engineering, Because you wanted to be alerted to

32:31 something's happened to you, right? you know that oh I'm having an

32:35 , I need to clean this We so alert you to that there

32:38 something going on there. OK? what happens is these um these uh

32:49 area so I can't get hit But, but what happens is let's

32:53 show the picture here. OK. here is the blood vessel in the

32:59 . So we we would have they were gonna kind of pull the

33:04 that make up the blood vessel apart little bit. So they can squeeze

33:07 . As you see, this neutrophil rolling down along the side of the

33:12 . There's actually little um uh uh help promote the uh release of these

33:20 surface molecules that kind of act like to kind of stop the neutrophils to

33:26 them down. Those are rolling Ok. And then, then the

33:32 uh cytokines kind of pull apart the of the blood vessel and that's how

33:35 squeeze through. So the um the uh squeezing through is the diapedesis.

33:43 . The kind of slowing down while stick to the surface before then is

33:47 margination. So, margination is kind , they stick to the cell wall

33:51 they squeeze out. That's the ok? Um Now, uh so

33:59 it's so, so as the neutrophils , right, exit the blood

34:03 of course, you're gonna have other come with it. It's not like

34:06 filter where only, only the neutrophils out, other stuff comes with it

34:10 that's what contributes to the, the . Ok? And uh then of

34:15 they're there in fighting infection. So have ptosis. So after a while

34:20 have what conforms pus pus is basically your white blood cells, some of

34:26 are still alive from the dead, cells that they, they die.

34:30 it's kind of collection of all that . Ok. Um And then uh

34:35 that's followed, of course, by and you may have some, depending

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

34:45 your movements impaired in the area or functions impaired until repair occurs. The

34:51 part is basically uh can be um cell division to replace the cells,

34:58 blood, uh scab formation, these of things. And so that leads

35:03 a what you see right here, can only lead eventually gets it clears

35:08 and back to normal. OK. let's um I'm gonna show this

35:16 Uh I'll come to this one in second. Uh Let's look here.

35:26 . So there we go. So is that's gonna be the same splinter

35:33 of uh example here. So you your vocabulary in the area. Villa

35:38 super tiny, uh one cell your red blood cells and mixed in

35:43 you see some neutrophils there, all white blood cells. So here's macrophage

35:48 here's the subcutaneous wound pathogens, here macrophages in the area. So remember

35:56 fixed macrophages, right? These these be sitting here just hanging out.

36:01 they have release of cyto contrast. that's the PTLR effect, right?

36:06 among the cytokines will be histamines et cetera. So we'll blow that

36:13 up. So here are cells that up the buzz vessel, OK?

36:17 for endothelial cell, then you have uh uh white blood cells will have

36:23 cells have these kind of glycoprotein of on the surface. And some of

36:27 are meant to, here's how it it down, right? It's rolling

36:30 , all right. And um then we have to break apart these

36:36 right? So don't worry about the here integra. Uh but these are

36:41 molecules and they interact with blood cell called ICANN to kind of help slow

36:46 down. Kind of analogous the velcro to those cells. And um then

36:55 have the effect of a Brady Yeah, that helps break apart the

37:00 between these cells uh temporarily, at so that they can uh slip

37:06 So the sticking part is kind of margination that what you just saw is

37:11 diapedesis or squeezes through. Ok. now they can get into the surrounding

37:16 and they can do their thing. use the size. OK.

37:21 and then of course, uh or come out and so you have more

37:27 , more histamine to kind of continue dilation effect and the, and the

37:33 and they have mass cells in the that all are triggered the youth hisam

37:36 , all to work on a blood causing dilation it. But then you

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

37:44 the area. Um And so the but again, this is classic

37:52 right? They work on the nerve to heighten the sense of pain in

37:56 area. And so you get your basic signs like redness, warmth,

38:03 , swelling, you can all the . So uh that's like inflammatory

38:10 acute inflammatory response, right? Um uh any questions about that? So

38:23 when this, when this can become uh bad for you. OK?

38:28 if um you have a, so talked about endotoxin before I grab negative

38:34 so that they lice and that materials that the material that cause a

38:40 Uh It's when you have a a think it has an inflammatory response that's

38:44 , not just they look less area body wide, right? So if

38:47 have a very negative infection in the , right, then potentially all the

38:52 in the much more cells in the can respond to this thing rather than

38:56 being a local effect, right? so knowing the effects of inflammatory

39:01 dying in blood vessels, right? If that happens on the body wide

39:06 , now you have blood vessels that gonna be, you know, being

39:10 and it's the flu coming out and blood volume will go down as a

39:14 because it's happening body wide, not locally and that's when you can go

39:18 the shot. And now you're using blood volume from numerous blood vessels in

39:23 body and uh blood pressure goes Um et cetera. So not a

39:29 thing. So, so a body inflammatory clots is something that's very dangerous

39:33 that happens. Ok. Um and endotoxin is one of those that can

39:38 this um ok, uh fever, ? So, fever is again something

39:49 all experienced. Um So it's really a resetting of a temporary resetting of

39:58 body's thermostat. Ok. So, , hypothalamus is what controls your body

40:05 . And, um, the, thing that will adjust the,

40:12 um, set point. So normally set point is at around 3738 or

40:19 , plus or my half a degree so, uh, we're all a

40:24 bit different but, uh, it's within that range. Um,

40:29 uh, and so what happens is triggers it to, to, to

40:35 ? Ok. And so pyrogens are chemicals that cause fever. Ok.

40:40 can have what's called endogenous or exogenous . Ok. So outside the

40:46 these are things like bacteria, viruses , they come into your body and

40:50 trigger endo endogenous pyrogens. So, you produce like introducing one or IO

40:59 , please act directly in the OK? And turn the set point

41:04 up and so, so a psych cycle if we take 37 C as

41:12 set point. Ok. Um So of pyrogens, uh can elevate

41:19 Ok. So if we go up say 40 give or take, um

41:25 shift to a higher set point. . So much like if um your

41:32 , when you go in front of house and you turn your thermostat.

41:36 . Um Are you going to immediately capable? You're gonna feel cool for

41:43 while, right? Until you're, that temperature gets to, to the

41:49 , temperature gets to what you said , right? So, So the

41:52 in your body, it's not So you turn a thermostat up in

41:56 body, it takes a bit for body to catch up with that new

42:02 point. And so until you you're gonna feel chilled. Ok.

42:08 Typically what happens is you kind of between chills and sweats, chills and

42:14 . Um because that, um that points kind of going up if you

42:21 of feel, feel the effects of as it goes down, your body

42:25 not, your body is at this set point, but it goes down

42:28 little bit and it takes a while readjust, you're gonna feel hot until

42:32 get to that new set point. that's why you go kind of typically

42:35 through oscillating high and low chills, and uh and uh sweats,

42:41 Until finally, you, you overcome infection, fewer breaks and you go

42:48 to your normal set point. Um Now you obviously, even,

42:54 though you o up your, when uh set point is increased and your

43:00 catches up with that temperature, you don't feel it obviously. Um but

43:05 is serving a purpose. OK. the most obvious is probably, you

43:10 , pathogens that affect our bodies, pathogens. Um You grow them at

43:16 degrees in, in the lab, ? So that's your body, that's

43:19 they're used to. So if you that, that that will affect their

43:23 growth rate. OK. So it that, but probably more importantly,

43:29 uh helps your immune system. So uh increases T cell activity.

43:34 one of the things about your adaptive system, right B cells and T

43:39 , they, they, they take , OK. So they have to

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

43:51 to that. OK. And so you can buy time to help them

43:57 , that's in your favor. And slowing down pathogen growth, retriver is

44:01 of those ways. So it, slows them down but enables your T

44:06 and B cells to find them and the engine and then do their

44:10 OK. So T cells as we , um a particular T cell type

44:16 very, it's kind of the master the whole, the whole thing,

44:20 ? Because there are B cells that to activated by T cells. B

44:23 make antibodies and T cells kind of with in intercellular pathogens. So,

44:29 the whole system is kind of regulated certain T cell types and you increase

44:33 activity to do this during fever. . And then iron uh again,

44:40 really goes back to thinking about right? What's needed for growth.

44:44 . Iron turns out to be a essential element for pathogens. OK?

44:50 for all life. But I uh you kind of fight with them

44:54 , over um the, the availability iron, right? You, you

44:58 many different ways, certainly through right. Hemoglobin, finding oxygen is

45:04 big source of iron, but also types as well. So you have

45:08 definite need for it and you need hold on to it. So,

45:11 you keep it away from pathogens that's affect their, grows as well?

45:17 , um, so fever does uh, definitely has a, a

45:23 in, in your innate immune which is still down to growth and

45:26 mobilize your adaptive immune system. Um, you know, too high

45:32 t, too high A T is not, that is detrimental.

45:37 ? Because your body can't sustain that something that's like 101102, you

45:41 that's sustainable. But uh but not you go with a 405 that's

45:46 your body can't function uh very well that. Ok. And obviously you

45:50 do something about that. But for of us that go through a typical

45:55 , you know, it's one that fever 101102 is, is typical.

46:02 . Uh For so compliment, so , um, is our protein factors

46:12 are not complement, are not a type? Ok. They're, they're

46:17 just proteins that are floating around in blood. Ok. And uh unless

46:22 until you're, until you have an , compliment is in an inactive

46:29 Ok. So there's ways to activate to make it do its functions.

46:36 ? And there are three ways that be triggered. Now, there are

46:40 bunch of proteins that make up OK? Uh But it really boils

46:46 to these, the C three and five, those when those get

46:53 that's generally when most of the action a compliment. OK. So

46:59 there's like 20 of these things that inactive and it's like a cascade

47:04 So, uh for example, C , you see there is inactive,

47:09 activated by I think C two, is from C three A and B

47:15 then activates five right into C five and B and it kind of goes

47:21 going. So C six activated in and 89. So that's, that's

47:25 you mean by cascade chain reaction. it's when these are activated. Like

47:31 said, that's when most of the occurs. OK. So um like

47:37 you have certain cell types that work the adaptive system, macrophages Andri cells

47:43 also work with the immune system. . So remember uh well, complement

47:50 classical path. This is the first bound. OK. So simply binding

47:57 uh a uh an antibodies activated. . You see antibodies bound here.

48:04 . And there's a compliment factor. so anybody binding to a pathogen,

48:09 compliment that activates the uh antibodies Now the effects you see here.

48:15 . Optimization cytolysis inflammation, those three when the compliments activated are the

48:24 But however, it is activated. are the three outcomes. OK.

48:28 , antibodies is one way to Um another way is to bind to

48:34 cell surface glyco lid. So, um have these old on surface.

48:44 . And complement can, can bind these. OK? And that in

48:49 can trigger the activation. OK. And then lastly is what I called

48:56 . OK. So, lectins are one of those Uh I mentioned

49:03 , tumor necrosis factor uh can go the liver and that can create the

49:08 to produce one of these c reactive . And, and uh lectin is

49:14 of those. OK. So, by it's very common uh nanos and

49:21 types of sugars are, are commonly on bacterial surfaces. OK? So

49:27 , that's what they find. And so uh that they can trigger

49:33 activation. OK. So um and again, the outcomes, you see

49:38 three outcomes here, ization, cytosis . So it's the same, the

49:42 three outcomes occur regardless of how it's . OK. So what are

49:46 what we know optimizations? OK. the, it's just uh like antibody

49:52 be a cell, the cell and cells can take up the pig cytic

49:58 can take it up. OK? cytolysis. So this you see here

50:08 complement proteins come together to form these channels in the cell membrane.

50:14 And basically the stuff leaks out of cell killing it OK. That's what

50:17 call a membrane attack complex. Maybe I put these complement proteins.

50:23 This is more effective with gram uh . OK? Because gram positive we

50:32 a couple of lighting cell wall OK? And so these don't really

50:38 into a cell wall, they fit a membrane. And so remember that

50:43 have a outer membrane layer. That's they're more susceptible to this kind of

50:47 . OK. And then uh is the uh inflammatory response. So

50:54 can um bind two cells in involved inflammatory response, releasing a histamine.

51:02 kind of enhance the uh th for response by producing these, triggering the

51:08 of these cytokines. OK. So , all three of these are are

51:14 of activating compliment no matter how it's . OK. Um And then uh

51:21 see interference. So, interferons uh think we talked a little bit about

51:27 in uh but they're a defense against . OK. Anti viral defense.

51:33 so we have different classes. Type is the one that's anti viral.

51:40 . And so how it works is this. OK. So you have

51:46 virus infected cell, OK. And have uh um that infection itself is

51:55 triggers the formation of uh interferon, . Iron effect and triggers that and

52:07 any neighboring cells OK. Cells in nearby nearby will, if they had

52:14 receptor for it will bind the, OK. Then those cells take it

52:19 and that acts as a activator to uh viral anti proteins. OK.

52:27 again, these are cells in the of this infected cell. OK.

52:34 um and the net result is the infection basically stops, right? Because

52:39 these uh cells uh have these antiviral that the virus comes in. They

52:46 block the infection. OK. So , the cell that starts infected is

52:52 likely succumb the infection. But the cells are then protected by uh by

52:58 action of interferon that they take Ok. So uh this was

53:07 I think. Um So it's like of the first biotechnology products to mass

53:12 to appear on it, anti viral . Um It didn't prove to be

53:19 because of the toxicity of it. in large doses, it's toxic.

53:23 it's not long lasting. Uh but is still effective um in the,

53:29 you go to the hospital and you a background infection, they do give

53:33 a neuron, a shot of neuron it is effective in kind of that

53:38 that setting, in a more local kind of way in a uh uh

53:42 , in and then start it uh small doses that works, it's affected

53:47 not as a marketing as a pill mass consumption. Doesn't, that doesn't

53:52 work. Ok. Nonetheless, it's, it's still it is effective

53:56 its its role. OK. Um other type of interfering is one that

54:04 neutrophils and macrophages. OK. So that means to activate a macrophage or

54:13 is it may initially look. So the key is that um it may

54:19 like this initially. OK. Then it's activated, it will have the

54:27 of these pseudopods. So that's an macrophage, for example. OK?

54:41 creating a pseudopod, he helps bind , and take things in,

54:47 To be creating more of those, really through the action of uh it's

54:51 that actually causes that. But that when you activate a ma,

54:55 there's different ways to activate, you do with interferon, you can do

54:58 with certain T cells. But that all the same. You create more

55:02 these pseudopods and that enhances vig. . Um So the uh antimicrobial

55:14 OK. Let's see. This yeah, this is the last last

55:19 the innate immune system that passes. . Um So these uh take different

55:27 . OK. So iron binding So remember that iron is a big

55:30 in terms of keeping away from pathogens slow their growth down. So we

55:34 things like transforms uh human level, don't bind iron is present.

55:40 But in actuality, pathogens also have kind of iron binding protein. That's

55:46 sara for. They bind specifically binding . Um the s uh antimicrobial

55:55 these are widespread uh various cells in bodies can produce these. OK.

56:01 kind of act like a uh uh me rock, they form a tunnel

56:06 in the uh the assembler form of in the some membrane causing lysis.

56:10 kind of like a membrane attack We just talked about uh this will

56:14 the type of the same kind of . It's really widespread what, what

56:19 can um attack, right? Not bacteria but different types of pathogens.

56:25 and sounding like macrophages, uh computer , other, other, other cell

56:31 in here, tissues in the So there's something like 50 or 60

56:36 more than that. There's like hundreds different varieties of these things um that

56:40 this antimicrobial activity that um so is so we're gonna recap this section and

56:51 a little bit about adaptive system. are there any questions about, we'll

56:56 about that response amps? What have ? OK. So let's look at

57:04 question here. Just kind of talked . I think all these things

57:09 OK. So which choice is Yeah. For transfers? Remember an

57:17 complex s interfere on type one C you. What? Try it

58:06 OK. All right. Counting down 15, 321. All right.

58:41 it is, choice is true is A is true. OK. That's

58:50 true one. Um Remember the tech is, that's comp a comp forms

58:58 um so complement can't figure size It's a, it's a protein.

59:04 . Um Interfer on type one. the antiviral amps or these antimicrobial

59:12 uh transference or iron binding uh Um OK. So there are a

59:21 in your book. Uh I think question electrolytes have kind of a summary

59:27 , here's the physical and chemical factors you like to use that. Uh

59:32 also a summary of the second line . Um You know, the uh

59:39 , you know, a lot of quiz this week, we give a

59:42 uh sampling the kind of questions you'll the same ones you've been seeing in

59:47 clip of questions. So, um let's talk a little bit. This

59:54 an overview about the immune system. get more into the details about it

59:59 time, but just for now, of setting it up. So this

60:03 third line defense is typically termed and T cells B cells and J.

60:09 also remember that macrophages interact. macrophages aren't technically part of this this

60:18 , but they interact with these cell , um dendritic cells, OK.

60:30 uh interact with T cells, Um So, um there's kind of

60:38 overview, so we call, we distinguish these two systems by human

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

60:49 . Um And each have their roles so uh there of course, are

60:54 types of li science BB type of type and T type lymphocytes. Um

61:02 cells kind of matured in the, both made in bone, but they

61:05 traveled to the thus where the T tr the thymus really developed uh and

61:10 T cells in the PAC system. but in terms of their, what

61:17 do, right? So B cells , they differentiate into what's called a

61:22 cell. And plasma cell is what the ABI OK. Memory cells.

61:27 remember there's memory, there's actually memory both. Your book doesn't really go

61:31 it. But and I'm not gonna you to know it, but there's

61:37 memory cells that are also part of T cells. So both sides have

61:40 memory component. OK? I'm most with the B cells that have the

61:45 component, uh vaccination, you get and if that if you get affected

61:51 the same antigen again, you'll produce . That's the memory memory component.

61:58 ? But there are special B cells that's what they become right? So

62:02 cells don't produce antibodies, the plasma do. OK? And the um

62:08 the end, the role B cells with extra c of attack.

62:14 So an antibody cannot go inside of cell and attack the antibodies only combined

62:21 pathogens that are outside of cells. . So um the T types T

62:29 types, they're what are called defector . And these deal with intracellular pa

62:35 . So uh they recognize cells are and they deal with them,

62:39 That's your cytotoxic T cells. Um these to be called, there's

62:45 type called inflator T cells, they typically become T helper cells. Uh

62:51 , um the uh other cell types T helper cells of other types,

62:57 like two types of T helper Basically one type activates um B

63:05 OK. Another type um activates macrophages dendritic cells. OK. So you

63:14 a differentiation between the two. Um Dendritic cells. OK. So

63:23 we'll see how A B cell works being activated. Typically, not

63:27 but usually activated by a certain type T cell T helper cell to produce

63:31 . And the macrophages and uh cells with other T helper cells to activate

63:37 . OK? Um And so the uh so antigens are antibodies.

63:46 So an antigen is typically gonna be it's of course, what, what

63:52 to an antibody? OK. And these are gonna be various types of

63:56 protein in nature, but they can lots of different chemical components, protein

64:03 can't be antigens. Um You think of what's on the periphery of

64:07 cell, right? It could be , it can be like lipids,

64:11 cetera, all can potentially be OK. So uh that's the thing

64:17 the adaptive immune system. It is stimulated by the presence of man.

64:23 it must be recognized, seen and bound to it and then stuff

64:29 OK. So uh so in terms the antibody, there's kind of two

64:36 to look at it. One is epitope. So the epitope is the

64:42 part of the energy that is OK. So we can see example

64:47 , this would be the gray, big gray block is the answer.

64:53 . That's what's recognized within that. antigen is the actual epitope shown in

65:00 , right? That's where the actual occurs, in fact. So antibody

65:06 antigen within it is an epitope where binding actually occurs. OK. And

65:13 , and there's a, there's as we'll see, although we don't

65:17 into the details of it because it's the immune response involving the death of

65:21 system is very complicated. OK? there's memory to it, there's actually

65:27 learning curve to it. So individual that are formed initially in response to

65:32 antigen uh actually get better at binning antigen as long as they keep getting

65:39 to it. OK. So the cells formed aren't, isn't as strong

65:44 terms of their immune response but gets . So there's also a learning curve

65:48 goes with it. So, um course, it all involves the chemicals

65:53 activated and things like that. But we're not gonna go into complex nature

65:58 it but kind of more overview. uh I guess the point I'm saying

66:03 that it's more complicated when I'm presenting you here. But you know,

66:08 this is this, this level is fine, right? This,

66:11 this will deal with what you need know. OK. Um But proteins

66:16 to be the best Ams in terms their, there's a lot of variety

66:19 protein, significant number of combinations that to be a type that energy is

66:26 tightly to, OK, less. with um carbohydrates and fat, just

66:32 the same variety of those types that are proteins. OK? Um And

66:40 antigenic determines, so ops, antigenic means the same thing. OK.

66:45 , um let's see. Any, stop, any questions, then we'll

66:50 ahead and stop there and we'll pick with finishing up couple 17 next

66:56

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