Adaptive Immunity

Hi. In this video we'll be talking about the adaptive immune system, which can mount a specific defense against pathogens. Now the crux of the adaptive immune system will revolve around the interactions between antigens, antigen receptors and antibodies. Those air like the let's call it the three A's of the adaptive immune system. And we've talked about antigens before those air molecules that will produce an immune response and specifically, uh, they will have a region or actually many regions, uh called Tepito pops that are basically parts of the antigen that could be recognized by the immune system and the parts that antibodies and antigens receptors will actually find. And again, you know, an antigen can have many different EP itto pops and different antibodies can, uh, recognize different Pepitone apps on a particular antigen. Now, antibodies are, uh, these why shaped proteins basically that are produced by B cells and will bind to antigens. And you can see that antigen antibody binding happening right there. Now, antigen receptors on B cells at least, are basically just like antibodies. That air stuck in the membrane and you can see a B cell receptor. There looks just like an antibody, except it has a trans membrane domain that is anchoring it in the cell membrane there. Now, T cell receptors are a little different than B cell receptors, and the way I think you should think of them is as if they're just like an arm of a B cell receptors. So, like, imagine this piece right here except stuck in the cell membrane over here. So, you know, here we have the membrane. Uh, it's anchored in right there. And here we have the binding site for the T cell receptor, so that's how I would think of it. And essentially, recognition will occur when B and T cells bind antigens. That's when our adaptive immune system recognizes a pathogen. So Theodore, active immune response has some special features. And that's, you know, that has to do with the fact that it is an antigen specific response and that, uh, it has Teoh be able to process and recognize specific pathogens. I mean, it's so specific that it can actually recognize different strains of the same pathogen and mount different responses to those different strains. So it the specificity just cannot be stressed enough. That's really one of the most important points of the adaptive immune system that it will essentially Onley bind to specific sites on specific antigens, and it mounts these very specific defenses now. It's also super adaptable. The adaptive immune system is really capable of recognizing an almost infinite diversity of antigens. It can, you know, specify itself to essentially, you know, almost anything encounters, obviously, some exceptions, but it's, you know, it's pretty incredible how flexible and adaptable it is. It also includes a type of memory, and this is super important because if you get infected with the pathogen you've already been infected with, your adaptive immune system is going to essentially be able to reactivate itself and mount the previous response that it developed for that pathogen very quickly in full force. And that's why if you get re infected with the pathogen that's already gotten you sick before, you probably won't even notice it because it won't have a chance to, like make you sick. Your adaptive immune system is just so on it now the last point, and you know this is one that's probably less obvious, but super important as well is something that we call self non self recognition essentially the ability of our immune system. Thio recognize the difference between pathogens and the cells of the organism, the self molecules and furthermore Uhh You know the adaptive immune system has thio ensure that you know molecules produced by the organism will never act as antigens. And we're gonna talk about how it does that little later. And here I just have, you know, basically wanted to show you guys the You know, the classic thing that's going on when you think of the adaptive immune system and that is B cells, uh, recognizing pathogens and producing tons of antibodies to combat them. You know, there's other stuff going on that we'll talk about. But, you know, let's say, like the main meat and potatoes is these B cells producing tons of antigens to counter act the infection. So with that, let's flip the page

The adaptive immune system is made of cells that can defend against specific pathogens, and the stars of the show are the T cells and the B cells. These air types of lymphocytes, which are cells found in limp, that clear fluid of the lymphatic system. And they also include natural killer cells which you might recall are part of the innate immune system. So T cells, as we'll see, are gonna be involved in what's called the cell mediated response, meaning they're going. Thio essentially helped destroy infected cells. They're gonna work on the cellular level, B cells are gonna be involved in the hue moral response, and their job is going to be to produce antibodies and secrete them into the humors of the body. It's very old fashioned term for the blood and lymph. You know, the fluids of the body. So they're gonna produce antibodies and secrete them throughout the body, which will help recruit immune cells and also fight the pathogens directly. Now lymphocytes are going to be produced in bone marrow like all Lucas sites and there going thio. Actually, T cells and B cells are actually going to mature in different places. T cells are going to move to the thigh. Imus to mature, which is a new Oregon, Uh, kind of like underneath the neck a little bit. You can see it right there on that picture, and B cells will actually stick around in the bone marrow to mature, so you can kind of remember it. Uh, you know this by t for thief Imus and B for bone marrow. Now, lymphocytes are named because they're the main type of self found in the lymph, and they circulate throughout the blood lymphatic system and spleen, which is a new Oregon that essentially filters the blood. It, uh, removes any damaged or dead or compromised red blood cells. And these lymphocytes will also hang out in lymph nodes, which filter. So they're basically gonna be hanging around all the places that, uh, you know, fluids of the body circulate through. And that's going to give them really good access to any pathogens that have found their way into the body. You know, there's a high probability that they'll run across them in these areas, and here you can see a layout of the lymphatic system. Uh, the lymph vessels connecting all the little lymph nodes as well as the organs like the spleen and the thymus. And here you have a new image of a lymph node. Jump out of the way here and you can see that if you, you know, zoom in. You can see, uh, lymphocytes floating around in there. And of course, uh, this lymph node is going thio have, uh, you know, a lot of lymph vessels flowing into it having their limp filtered, and then the limp will flow out of the note and continue flowing through the lymphatic system, and some fluid will actually re enter the bloodstream. Now, there's also this tissue type called mucosal associate associated lymphoid tissue or malt. And basically, this is thes air immune system cells that are going to be found in the gut and the respiratory tract. These, uh, tissues that are gonna be mucus e to scoop up any invading pathogens. And, you know, they're not labeled here in this image. But I want to bring your attention to them because, you know, they are, you know, they are part of this immune system and, uh, you know, they do play an important role in picking up any pathogens that air trying Thio enter the body. Now with that, let's flip the page

every B and T cell is going to have a single type of antigen receptor, and that's going to be specific. Toe a single type of Auntie Jen here you can see an example of this. We have different B cells, each with a specific type of B cell receptor that is meant for a specific type pathogen. Now, immuno globulin are going to be the class of proteins that include antibodies and B cell receptors. And there's actually five classes. You don't need to worry about knowing these names. I just throw them in there in case you're curious. And essentially, what I want you to know is that each is a type eso each, you know, subtype that you see here is gonna have ah, unique heavy chain and function. What is a heavy chain? We're gonna get to that in a second. So the B cell receptor is has the same structure is the antibodies produced by those B cells and it's gonna be made up of what were called heavy chains and light chains, two of each, actually too heavy chains to light chains. The light chain is the smaller of the poly peptides and the heavy chain is the larger, and this terminology also applies to antibodies. It's not just specific for B cell receptors. So here, looking at RB cell receptor, these little pieces that you see on either side, those are the light chains, and these bigger pieces that you see here and here will draw a red line through them just to be super crystal clear. Those bigger pieces, those oops are the heavy chains. And as I've said before, you know, the only real difference between the B cell receptor and antibodies it produces is that the B cell receptor is gonna have a trans membrane domain. Now, T cell receptors are gonna be fairly similar in structure to like one of the arms of immuno globulin. And it's going to instead of being made up of a heavy chain and a light chain gonna be made of what we call an Alfa chain and abated chain. And I'm gonna jump out of the way here and you can see that we have a T cell receptor right here T cell receptor, and it has its Alfa chain and its beta chain, and it's kind of like just one of these arms from the B cell receptor from an antibody. And here is its binding site. And here is the anchor into the membrane. And the main difference between these B cell receptors and T cell receptors on this is something we're gonna talk about more in just a moment is that B cell receptors will actually bind directly to antigens. But T cell receptors on Lee bind to antigens that are presented on the surfaces of other cells in process known very creatively as antigen presentation. So with that, let's actually flip the page.

As I've said before, a single antigen can have many different EP itto pops in its structure. B cell receptors will bind to EP itto pops on complete antigens. But T cell receptors bind Tepito piece that have been processed and presented, and the key to this episode binding. And the specificity of the adaptive immune system lies in the genetics of the antigen receptors, and it has to do with what are called constant regions and variable regions. So constant regions, as the name implies, remain constant. And those are parts of the light chain and heavy chain and the alfa and beta chains. Depending on whether you're talking about B cell receptors or T cell receptors, that will be the same in each is a type of that receptor, and here you can see those highlighted in these darker regions. So these are going to be the constant regions or, well, just abbreviate it. See regions, whereas these lighter colored regions chow mark and red just to be extra clear thes air going to be our variable regions or V regions. So how does this all work? How do these variable regions vary from cell to cell? Well, the genes for antigen receptors have many V regions, actually, and they also have other types of regions and thes regions will recombine in unique ways to produce unique structures. This is, uh, kind of the key to how these antibodies and ancient receptors get that specificity to an antigen. So, for example, with light chain actually has about 40 variable regions Azaz well as what are called five joining segments. And between these alone, you can get over to our sorry not over exactly 200 possible combinations. So huge amount of variation there actually, other regions involved that add more variation. But that's kind of beyond the level of understanding that we need. So what happens is as lymphocytes mature, uh, there's genetic recombination of the various regions that will result in unique antigen receptors. And essentially, this genetic recombination is, you know, the crux of the specificity and flexibility of the adaptive immune system. And, uh, what's so amazing? Getting back to that self non self recognition we talked about is that if maturing B and T cells have antigen receptors that bind to self molecules, they are destroyed or deactivated. So the adaptive immune system has a way of guarding against, you know, a T cell or B sell accidentally developing a type of antigen receptor that would bind to a self molecule or molecule Or, you know, a cell of the organism's body. Pretty incredible stuff. And here you can see that recombination sort of modeled out. You know, I don't really want you to worry about the specifics. All you need to know is that there's, you know, a variety of regions that are essentially mixed and match thio create unique receptors. So with that, let's flip the page.

T cells and B cells become activated when they're antigen receptors. Bind the appropriate Auntie Jen, and basically these lymphocytes just flow and hang out around the lymphatic system, the blood, the spleen and some even in the skin, and that mucosal associated lymphoid tissue. Until they get a match. It's It's kind of a scattershot approach that the adaptive immune system takes. They try as many different things as they can, and if they get a hit, that's great. But if cells don't encounter the proper EP itto within a certain timeframe, they'll actually die. Cells will eventually die, and if they do encounter the right Apatow, though, they will basically clone themselves. They'll divide and turn, create a what's called a clonal population just a big group of Selves that are clones of them. And this is part of what's called clonal selection theory. Essentially, this is an idea that says antigens will basically select the lymphocytes by, you know, the lymphocyte. Just encountering the right Auntie Jen, the antigens will select the lymphocytes to divide into that clonal population. So basically, you know, if they are activated, they will make a you know, many clones and, uh those clones will become what are called defector cells and memory cells. And before we talk about what those are, I do want to point out that sometimes, uh, lymphocytes that have not been exposed to an antigen yet are called naive lymphocytes. So that's just a mature lymphocyte that hasn't yet been exposed to It's appropriate. Auntie Jen. Now affect our cells are gonna be the short lived but fast acting, um, cells of the adaptive immune system. They're going to take immediate action against the pathogens that are present. Memory cells are gonna be longer living cells. They actually will continue Thio divide at a low rate thio keep up a population around, and they're going to just hang around and be used to fight future infection. So their job is not to take action against these current pathogens. Invading their job is to wait and see if they come back and then mess those dudes up. And here you can kind of see unexamined of how this sort of clonal selection it goes down. We have these, like naive lymphocytes. This particular one has a match. So it's going Thio clone itself a bunch. Uh, these other guys, they didn't get matches, so they're gonna die out. Sorry. You know, brutal in the immune system. And this clonal population is going to divide between some memory cells. And some affect your cells that you can see behind me. All right with that, let's flip the page.

before we can get into what B and T cells do, we need to talk about how cells display antigens. And this involves these proteins called major history compatibility, complex proteins or just the major history compatibility complex. Or because that's such a mouthful, MHC. That's what I'm going to call it from now on. So these were just cell surface proteins that will display antigens. And, uh, this process is known as Auntie Jen Presentation this displaying of antigens at the cell surface using these MHC proteins. So there's actually gonna be two classes of MHC proteins that we're gonna be concerned with. Class one are actually expressed by all cells of the body, and these almost act like a window into the cell. They display antigens that air found inside that cell. So this is a way that cells can alert the immune system thio an infection inside of that cell. Uh, this is also the reason that organ transplants, uh, will be rejected by the immune system because the foreign Oregon will display different MHC one proteins. And here you can sort of see unexamined alot of what it might look like. This type of antigen presentation so some anti agent could be like whole pathogen will get inside the cell. The MHC class one protein inside the cell will bind to it and moved to the surface and display it there. Now MHC class two proteins are expressed by antigen presenting cells. Remember those air the cells that display antigens that air found? And, uh, I'm sorry, those air cells that display antigens that are involved in the adaptive immune system and those are going to include dendritic cells, the bridge between the adaptive and innate immune system, macrophages and B cells. So these MHC class two proteins will display antigens that air actually found outside of the cell, then collected and brought inside the cell. So these antigen presenting cells remember dendritic cells and macrophages are faggots sites. So they'll faggot faggot Saito's some Auntie Jen, bring it in, bind it to an MHC to protein, and then bring that to the cell surface and present that Auntie Jen at the membrane. So dendritic cells do this with a special purpose because they are actually going thio, grab these antigens and then kind of run thio other immune cells to sort of like tattle on them being like, Look here, here's Ah, pathogen, I found. And they're actually going Thio not just faggots Ito's antigens, but actually then degrade them into uhh, you know, little fragments. And it's actually gonna be those fragments that they display with the MHC Class two proteins. So, you know, in this image, it looks like it's a whole bacterial cell. But in reality, you know, a dendritic cell would just be displaying some fragment from that bacterial cell, some fragment that would act as an anti gin. So with that, let's flip the page.

previously we said that b cells can encounter antigens that are just free floating in the body. But t cells need to be presented antigens and T cells are actually going to be classified as either Cd four plus or Cd eight plus based on whether they have a cd four or cd eight protein. Now these CD four Plus T cells Will interact with epic tokes bound to MHC Class two proteins. You can see this happening here and uh those MHC class two proteins remember are going to be found on antigen presenting cells like dendritic cells. And uh when these Cd 84 plus T cells are presented with Epic Tokes that they can interact with, they become activated. And these activated Cd four plus T T cells will undergo clonal expansion and form helper T cells. And uh the Cd eight plus T cells will interact with Pepitone apps on MHC one class proteins which are going to be found on most cells. So uh you know these aren't gonna be those specific antigen presenting cells like the dendritic cells and the B cells and the macrophages. Instead these are going to be found on just like your average regular joe sells. And it's going to if they combined to those episodes it's gonna activate those Cd eight plus T cells and those will undergo clonal expansion to form side a toxic T cells. So here behind me you can see the side a toxic T cells being formed from antigen presentation with an MHC one Class protein. And over here you can see helper T cells being formed from an interaction with an MHC class two protein. And remember these are going to be the antigen presenting cells like dendritic cells. No, basically what these guys are asking is show me what you got. So let's talk about what these types of cells do side a toxic T cells which sometimes abbreviated T. C. These are effect er T cells. And their job is to kill pathogen infective cells. This is basically a defensive measure against the pathogen. So if this cell, let's say uh has been infected and it is presenting the antigen from that pathogen, the psycho toxic or killer T cell will come over and induce cell death. It will induce uh you know the cell to die with that. Let's flip the page and talk about what helper T cells do.

helper T cells are the other type of effect, or T cells, and their role is to assist with the activation of other immune cells and to recruit other immune cells by secrete ing side kinds. There's actually two types there, th one cells whose specific role is to activate those site a toxic T cells. And there are th two cells whose specific role is to help activate B cells, which we'll talk about in just a moment. I just want to quickly point out this diagram of a helper T cell, which, if it encounters theater pro pre it the appropriate MHC UH, appropriate antigens bound thio MHC uh, protein. It's going thio respond by, you know, either activating B cells, macrophages or T cells or releasing cited kinds to attract other immune cells. That's what's going on in this image. Now B cell activation occurs when a B cell receptor interacts with a free floating auntie gin that has an EP itto it combined thio, and it will find these in the lymph or in the blood now that Auntie Jen, when it's bound to the B cell receptor, will be ingested into the cell, then digested and then part of it will be attached to an MHC Class two protein and transported to the cell surface, where it will be displayed. Now, th two cells that have complementary receptors to the displayed antigen will bind to the B cells, and this TH to sell will be activated by that interaction with the B cell, and it will cause it to release cytokines. And those CIDA kinds will then in turn stimulate that B cell so they'll basically they'll have an interaction where they stimulate each other. They kind of complement each other and stimulate each other. And this causes the B cell to become fully activated. And when it's fully activated, it's going to replicate and generate effect er and memory cells. That's what's going thio, you know, cause the B cell Thio, you know, produce those clonal populations. And in that process, those B cells will experience what's called somatic hyper mutation. Essentially, it's just like, ah, lots of mutation, but kind of like planned for mutation. I don't want to say controlled mutation, but it's like the the cells induced this mutation, and it allows those replicating B cells toe actually fine tune the receptor to bind the antigen. Better now. Thes fully activated B cells. Air going Thio, as we said, produce effect er and memory cells. The effect, er cells are some of the effect er sells it Will producer called plasma cells these air effect er B cells that produce massive amounts of antibodies and secrete those antibodies into blood. They're basically antibody factories, and you can see here this whole process, the B cell encounters the appropriate Auntie Jen. You see this B cell can't bind that Auntie Jen, so it's not gonna be activated. And then the B cell has an interaction with the Helper T cell, which causes it to become plasma cell and produced tons of antibodies and then secrete them into the blood. So that's the basic idea behind how thes B cells they're going to do their job. Let's flip the page

antibodies can affect pathogens in a variety of different ways, one of which is called optimization, which essentially is when pathogens that have antibodies bound to them are more easily targeted and removed by macrophages and neutrophils. Essentially, the antibody, which binds the antigen on the on the pathogen, makes it easier for the faggots site. Faggot sites Thio come over and identify and then digest those particular pathogens. Now antibodies can also neutralize pathogens in the sense that if they coat theme, the um, they coat the pathogen, you know, and coat its exterior to the point where it basically can't function anymore. It can't infect the host cell because it's just covered in antibodies. It's like, uh, they form a shield around it, preventing it from interacting with anything in the body. This is kind of a similar idea to a glue tenacious, which is basically how antibodies can lead to clumping uh, antibodies. You might recall, or why shaped, and they have to binding sites, right? So if one binding site, let's say, binds one pathogen and another binds a different pathogen, and then another antibody binds that pathogen and another one and so on, and so forth. These antibodies can basically create big clumps of pathogens. That air kind of just stuck in this matrix of antibodies. And this, uh, you know, leads to clumping and basically rendering these, uh, pathogens neutralized. And you can see this clumping happening here and here on these particular samples. So, uh, this anti a anti be anti D That's referring to types of antibodies. And, you know, basically what's happening is the anti a antibody eyes causing a gluten nation in this sample in the anti D antibodies causing a gluten nation in this sample. But the anti B isn't binding. There's no no binding there. So no, a gluten nation. Um, but you can actually see the clumping. It's pretty wild, right? Like these samples should look like this sample for anti B, but, uh, you can see that the material which would give it that solid color all the way through, is all clumped together now. Lastly, we talked about complement proteins, and we talked about the innate immune system, and I said that not only can these be activated by pathogen associated molecular patterns, but they could be activated by antibodies to create holes in pathogen membranes, so these complement proteins are also going to be part of the adaptive immune system and are going to respond to antibodies now. As I said, the adaptive immune system kind of has two sides to it. The cell mediated response, which is going to occur through cell to cell contact and is mainly going to involve site a toxic T cells, which will be promoted by those th one cells remember their job is to help activate those side of toxic T cells. There's also the the hue moral response, which eyes going to occur in the blood and lymph or the humors of the body. And it's going to involve antibodies being released from plasma cells, which are promoted by those th two cells. So those air basically like the two aspects of the adaptive immune system, the cell to cell, uh, you know, cell to cell battle and the battle in the blood if you want to think about it that way. Now we have talked about what these affect our cells do. But remember, there's also those memory cells that are being produced, and their job is to deal with the secondary immune response primary immune response is what happens the first time you encounter an infection. And, uh, you know, antibodies are produced in response to that infection. And as you can see in a primary immune response, the amount of antibodies produced is not nearly as much as you see in a secondary immune response. And that's because the system is actively, you know, trying to identify and fight this infection. The secondary immune response is, you know, so much more powerful and potent. You see, there's, you know, there's less of a lag. Uh, in the secondary mean response. The antibody concentration shoots up almost instantaneously because it's activating those memory cells. Those pathogens are activating those memory cells now. This all is part of what we call active immunity, where you know you get an infection and you produce antibodies is part of a primary or secondary immune response. But it's worth noting that there's also what's called passive immunity, which is when you actually receive antibodies from another individual to help you deal with an infection. This is worth noting because that's how fetuses deal with infections. Mothers will actually pass on antibodies to their fetuses to help them fight off any infections they have encountered while they're developing. So that's all I have for this page. Let's flip the page.

modern medicine has allowed us to really manipulate our technology to mount better defenses against pathogens. We basically have found ways to manipulate our own immune systems to save us the trouble of getting sick. We call this immunization, which is basically when an organism's immune system gains. The specific defense against some pathogen is usually happens through what's called vaccination. Vaccination is going to be the introduction of a vaccine to prime the immune system. Thio deal with later infections. Basically, it allows you to mount a primary immune response. Thio some weekend or killed form of pathogen. That's not actually going to get you sick so that if you ever in the wild, so to speak, encounter you know that nasty bug in its, uh, form where it can actually get you sick, you have a secondary immune response ready to go to beat it down. A vaccine is a biological preparation that contains antigens, and, as I said, usually it's like a weakened or killed form of a pathogen. The name comes from the Latin word for cow, which is vodka and essentially, uh, if you're wondering why this has anything to do with cows, it's because the first, uh, you know, a famous case of vaccination in Western medicine anyways, was with this guy right here. His name is Edward Jenner, and he used the, uh, cowpox virus to vaccinate people against smallpox, which was a rampant and deadly disease. It was pretty gnarly how he did it. I mean, he literally took basically a two pronged needle that looked like that and dipped it in a vial of cowpox so that a liquid droplet would kind of stick between the two prongs, and then he would just prick you with it. And, you know, make sure that some of that liquid gets into your blood Pretty gnarly stuff. But it worked. And this would actually be an example of a type of vaccine that contained what's called an attenuated virus. Basically, uh, it's an infectious virus that's cult cultured in a species other than a host, so it won't infect the host cells. This is not exactly an intent attenuated virus because, you know, cowpox is its eyes, its own disease, but it's highly related to smallpox. It's just that it infects cows instead of humans. So very similar idea to an attenuated virus. You can also see vaccines that air called sub unit vaccines that contain isolated viral proteins. So, basically, you know, some scientists will, uh, take a virus and break it down and find some good antigens to use and then, uh, inject you with that so that you can recognize the antigens, but you never actually have to have the virus inside you. You can also get an inactivated virus, which will be like a damaged virus that contains antigens but can't cause infection now, often in, uh, you know, biotechnology, you'll see things called monoclonal antibodies used. And these air just antibodies that air prepared from a single clone of B cells. Uh, you know, specific for some epic tope. And you know, these will be used often in in research for many, many different purposes. But you probably will see that name come up now. You know what it iss now? Things could go wrong with the immune system. Allergies are common example of an abnormal immune response. Thio Ananta gin, which will call an allergen. Basically, it's not something that's actually going to get you sick, but your body still mounts an immune response to it. You know, That's why, for example, if you're allergic to cats or something, you know, uh, the cat dander will make you, um, sneezy. You can get that inflammatory response right. You'll get all swollen and puffy. Um, it's just your immune system going a little overboard, right? Identifying something is a threat that's not actually a threat now allergies. Air unpleasant, but they're not nearly as dangerous as auto immunity, which is when a new immune response is directed at self molecules and the cells of the organism. Essentially the cells of your immune system attack and kill your own body, for example, and diabetes mellitus it, you know, can be caused by an auto immune reaction that has the immune system specifically target the cells that and target and kill the cells that produce insulin. And that's why people with that, uh, condition can't produce insulin even though they have a pancreas because their immune system, you know, went haywire and just killed those insulin producing cells in the pancreas. Now, HIV or human immunodeficiency virus is a very heavily researched virus that infects and kills CD four plus T cells and macrophages. And this is, uh, you know, obviously very dangerous because it's a virus that actually targets and attacks the adaptive immune system, which is really bad news because it it essentially, can prevent your immune system from being able to mount a new immune response not only against it, but other pathogens as well. Uh, you know, those helper T cells, which are the CD four plus T cells are needed for both the hue moral response and the cell mediated response. Remember, they're gonna help activate site a toxic T cells, and they're gonna help activate B cells to produce antibodies. So basically, this virus attacks. You know, the most one of the most vulnerable cells of the immune system. If you want to just take the whole system out now, there's a condition that develops from HIV that we know as AIDS or acquired immune deficiency syndrome. Basically, this is a It's not a separate disease. It's, ah, severe weakening of the immune system from an HIV infection. If you have an HIV infection, uh, for a long time or it's untreated for a while or something, it can lead to your immune system getting so weak that you can't fight off any infections any little thing can get you sick to the point where it can kill you. And that is, you know, sort of how HIV isa lethal diseases. It just takes out your immune system so that, even like a little cold or something, uh, could could be fatal. And here, uh, not to end on to darken out. But here you can see, uh, a cell being attacked by HIV virus. So with that, it's all I have for this lesson. Stay healthy, guys. But if you get sick now, you know what your body is doing to fight against it.