Adaptive Immunity: Videos & Practice Problems

The adaptive immune system, featuring B cells and T cells, mounts specific defenses against pathogens through antigen recognition. B cells produce antibodies that bind to antigens, while T cells require antigen presentation via major histocompatibility complex (MHC) proteins. Activation leads to clonal expansion, forming effector and memory cells, enhancing the immune response. This system distinguishes self from non-self, ensuring effective pathogen targeting while preventing autoimmunity. Immunization primes the immune system for future encounters, exemplifying active immunity, while passive immunity involves antibody transfer from one individual to another.

Adaptive Immune Response

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 are like the let's call it the 3 a's of the adaptive immune system. And we've talked about antigens before. Those are molecules that will produce an immune response and specifically, they will have a region or actually many regions, called epitopes that are basically parts of the antigen that can be recognized by the immune system and the parts that antibodies and antigen receptors will actually bind. And again, you know, an antigen can have many different epitopes and different antibodies can, you know, recognize different epitopes on a particular antigen. Now, antibodies are, these y-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 are stuck in the membrane and you can see a B cell receptor there looks just like an antibody except it has a membrane domain that is anchoring it in the cell membrane there. Now, T cell 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 receptor. So like, imagine this piece right here except stuck in the cell membrane over here. So, you know, here we have the membrane, 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, the adaptive 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, it has to 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, 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 only bind to specific sites on specific antigens and it mounts these, you know, very specific defenses. Now, it's also super adaptable. The adaptive immune system is really, you know, capable of, you know, recognizing an almost infinite diversity of antigens. It can, you know, specify itself to, essentially, you know, almost anything it 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 a pathogen you've already been infected with, your adaptive immune system is going to essentially be able to reactivate itself and combat the pathogen very quickly in full force. And that's why if you get reinfected with a pathogen that's already gotten you sick before, you probably won't even notice it because it 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, to recognize the difference between pathogens and, you know, the cells of the organism, the self molecules. And furthermore, you know, the adaptive immune system has to ensure that, you know, molecules produced by the organism will never act as antigens and we're going to talk about how it does that a 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 recognizing pathogens and producing tons of antibodies to combat them. You know, there's other stuff going on that we'll talk about but the, you know, let's say like the main meat and potatoes is these B cells producing tons of antigens to counteract the infection.

So, with that, let's flip the page.

Lymphocytes

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 are types of lymphocytes, which are cells found in lymph, 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 going to be involved in what's called the cell-mediated response, be involved in the humoral response, and their job is going to be to produce antibodies and secrete them into the humors of the body. It's an old-fashioned term for the blood and the lymph, you know, the fluids of the body. They're going to produce antibodies and secrete them throughout the body, which will help recruit immune cells and also fight the pathogens directly.

Lymphocytes are going to be produced in bone marrow, like all leukocytes, and T cells and B cells are actually going to mature in different places. T cells are going to move to the thymus to mature, which is an organ, kind of like underneath the neck a little bit. You can see it right there in that picture and B cells will actually stick around in the bone marrow to mature. So, you can kind of remember it, you know, by T for thymus and B for bone marrow.

Lymphocytes are named because they are the main type of cell found in the lymph, and they circulate throughout the blood, lymphatic system, and the spleen, which is an organ that essentially filters the blood. It removes any damaged, dead, or compromised red blood cells, and these lymphocytes will also hang out in lymph nodes, which filter lymph, so they're basically going to be hanging around all the places that, you know, fluids of the body circulate through, and that's going to give them a really good access to any pathogens that have found their way into the body. 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, the lymph vessels connecting all the little lymph nodes as well as the organs like the spleen and the thymus. And here you have an image of a lymph node. Jump out of the way here. And you can see that if you zoom in, you can see lymphocytes floating around in there, and, of course, this lymph node is going to have a lot of lymph vessels flowing into it, having their lymph filtered, and then the lymph will flow out of the node 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-associated lymphoid tissue, or MALT, and basically, these are immune system cells that are going to be found in the gut and the respiratory tract. These tissues are going to be mucusy to scoop up any invading pathogens, and, you know, they are not labeled here in this image, but I want to bring your attention to them because they are part of this immune system and play an important role in picking up any pathogens.

Now, with that, let's flip the page.

Antigen Receptors

Every B and T cell is going to have a single type of antigen receptor, and that's going to be specific to a single type of antigen. 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 of pathogen. Included are antibodies and B cell receptors, and there are actually 5 classes. You don't need to worry about knowing these names. I throw them in there in case you're curious, and, essentially, what I want you to know is that each isotype, so each, you know, subtype that you see here, is going to have a unique heavy chain and function. What is a heavy chain? We're going to get to that in a second. So, the B cell receptor has the same structure as the antibodies produced by those B cells, and it's going to be made up of what are called heavy chains and light chains. 2 of each, actually. 2 heavy chains, 2 light chains. The light chain is the smaller of the polypeptides, 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 our B 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, I'll draw a red line through them just to be super crystal clear. Those bigger pieces, those are the heavy chains. And as I've said before, you know, the only real difference between the B cell receptor and the antibodies it produces is that the B cell receptor is going to have a transmembrane domain. Now, T cell receptors are going to be fairly similar in structure to, like one of the arms of an immunoglobulin, and instead of being made up of a heavy chain and a light chain, it's going to be made of what we call an alpha chain and a beta chain. And, I'm going to 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 alpha 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, and this is something we're going to talk about more in just a moment, is that B cell receptors will actually bind directly to antigens, but T cell receptors only bind to antigens that are presented on the surfaces of other cells in a process known very creatively as antigen presentation. So with that, let's actually flip the page.

Constant and Variable Regions

As I've said before, a single antigen can have many different epitopes in its structure. B cell receptors will bind to epitopes on complete antigens, but T cell receptors bind to epitopes that have been processed and presented. The key to this epitope 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 alpha and beta chains depending on whether you're talking about B cell receptors or T cell receptors. That will be the same in each isotype of that receptor and here you can see those, highlighted in these darker regions. So, these are going to be the constant regions, or we'll just abbreviate it, C regions. Whereas these lighter colored regions, which I'll mark in red just to be extra clear, these are 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 these regions will recombine in unique ways to produce unique structures. This is kind of the key to how these antibodies and antigen receptors get that specificity to an antigen.

For example, the light chain actually has about 40 variable regions, as well as what are called 5 joining segments, and between these alone, you can get over 2, or sorry, not over, exactly 200 possible combinations. So, a huge amount of variation. There are 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, there's genetic recombination of the various regions that will result in unique antigen receptors. And essentially, this genetic recombination is the crux of the specificity and flexibility of the adaptive immune system. And 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 a T cell or a B cell accidentally developing a type of antigen receptor 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 a variety of regions that are essentially mixed and matched to create unique receptors.

So with that, let's flip the page.

Clonal Selection Theory

T cells and B cells become activated when their antigen receptors bind the appropriate antigen. Essentially, these lymphocytes just flow and hang out around the lymphatic system, the blood, the spleen, and some even in the skin and mucosal associated lymphoid tissue until they get a match. It's a kind of 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 epitope within a certain time frame, they'll actually die. Cells will eventually die. And if they do encounter the right epitope though, they will essentially clone themselves. They'll divide and turn, create what's called a clonal population. Just a big group of cells that are clones of them. This is part of what's called clonal selection theory. Essentially, this is an idea that says antigens will basically select the lymphocytes by the lymphocyte just encountering them and, if they are activated, they will make many clones and those clones will become what are called effector cells and memory cells.

Before we talk about what those are, I do want to point out that sometimes 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 its appropriate antigen. Now, effector cells are going to be the short-lived but fast-acting cells of the adaptive immune system. They're going to take immediate action against the pathogens that are present. Memory cells are going to be longer-living cells. They will continue to divide at a low rate to keep up a population and they're going to hang around and be used to fight future infections. 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. Here, you can kind of see an example of how this sort of clonal selection goes down. We have these naive lymphocytes. This particular one has a match. So it's going to clone itself a bunch. These other guys, they didn't get matches so they're going to die out. Sorry. It's brutal in the immune system and this clonal population is going to divide between some memory cells and some effector cells that you can see behind me. Alright, with that let's flip the page.

Major Histocompatibility Complex

Before we can get into what B and T cells do, we need to talk about how cells display antigens, and this involves proteins called major histocompatibility complex proteins, or just the major histocompatibility complex, or because that's such a mouthful, MHC. That's what I'm going to call it from now on. So, these are just cell surface proteins that will display antigens, and this process is known as antigen presentation, this displaying of antigens at the cell surface using these MHC proteins. So, there's actually going to be 2 classes of MHC proteins that we're going to be concerned with. Class 1 proteins are actually expressed by all cells of the body, and they almost act like a window into the cell; they display antigens that are found inside that cell. This is a way that cells can alert the immune system to an infection inside of that cell. This is also the reason that organ transplants will be rejected by the immune system because the foreign organ will display different MHC 1 proteins. And here, you can sort of see an example of what it might look like, this type of antigen presentation. Some antigens, you know, could be like whole pathogens, will get inside the cell. The MHC class 1 protein inside the cell will bind to it and move to the surface and display it there. Now, MHC class 2 proteins are expressed by antigen-presenting cells. Remember, those are the cells that display antigens that are found in, I'm sorry, those are 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 systems, macrophages, and B cells. So, these MHC class 2 proteins will display antigens that are actually found outside of the cell, then collected and brought inside the cell. So, these antigen-presenting cells, phagocytes. So they'll phagocytose some antigen, bring it in, bind it to an MHC 2 protein, and then bring that to the cell surface and present that antigen at the membrane. So, dendritic cells do this with a special purpose because they are actually going to grab these antigens and then kind of run to other immune cells to sort of like tattle on them, being like, "Look here, here. Here's a pathogen I found," and they're actually going to not just phagocytose antigens, but actually then degrade them into little fragments, and it's actually going to be those fragments that they display with the MHC class II proteins, so, you know, in this image it looks like it's a whole bacterial cell but in reality, a dendritic cell would just be displaying some fragment from that bacterial cell, some fragment that would act as an antigen.

So with that, let's flip the page.

Antigen Presentation and Cytotoxic T Cells

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. T cells are actually going to be classified as either CD4⁺ or CD8⁺ based on whether they have a CD4 or CD8 protein. Now, these CD4⁺ T cells will interact with epitopes bound to MHC class 2 proteins. You can see this happening here. Those MHC class 2 proteins, remember, are going to be found on antigen-presenting cells like dendritic cells. When these CD8⁺ T cells are presented with epitopes that they can interact with, they become activated. These activated CD4⁺ T cells will undergo clonal expansion and form helper T cells.

The CD8⁺ T cells will interact with epitopes on MHC class 1 proteins, which are going to be found on most cells. So, you know, these aren't going to 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 cells. If they can bind to those epitopes, it's going to activate those CD8⁺ T cells, and those will undergo clonal expansion to form cytotoxic T cells. So here behind me, you can see the cytotoxic T cells being formed from antigen presentation with an MHC class 1 protein. And over here, you can see helper T cells being formed from an interaction with an MHC class 2 protein. Remember, these are going to be the antigen-presenting cells, like dendritic cells. Now, basically, what these cells are asking is, "Show me what you've got."

Let's talk about what these types of cells do. Cytotoxic T cells, which are sometimes abbreviated as TC, are effector T cells, and their job is to kill pathogen-infected cells. This is basically a defensive measure against the pathogen. So, if this cell, let's say, has been infected and it is presenting the antigen from that pathogen, the cytotoxic or killer T cell will come over and induce cell death. It will induce the cell to die.

With that, let's flip the page and talk about what helper T cells do.

Helper T Cells and B Cells

Helper T cells are the other type of effector T cells and their role is to assist with the activation of other immune cells and to recruit other immune cells by secreting cytokines. There are actually two types. There are Th1 cells whose specific role is to activate those cytotoxic T cells, and there are Th2 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 the appropriate MHC, or appropriate antigen bound to the MHC protein, it's going to respond by either activating B cells, macrophages, or T cells or releasing cytokines 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 antigen that has an epitope it can bind to and it will find these in the lymph or in the blood. Now, that antigen, 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 2 protein and transported to the cell surface where it will be displayed. Now, Th2 cells that have complementary receptors to the displayed antigen will bind to the B cells and this Th2 cell will be activated by that interaction with the B cell and it will cause it to release cytokines and those cytokines will then, in turn, stimulate that B cell. So they'll basically have an interaction where they stimulate each other. They 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 effector and memory cells. So, that's what's going to, you know, cause the B cell to, you know, produce those clonal populations and in that process, those B cells will experience what's called somatic hypermutation. Essentially, it's just like lots of mutation but kind of like planned for mutation. I don't want to say controlled mutation but it's like the cells induce this mutation and it allows those replicating B cells to actually fine-tune the receptor to bind the antigen better.

Now, these fully activated B cells are going to, as I said, produce effector and memory cells. The effector cells, or some of the effector cells it will produce are called plasma cells. These are effector B cells that produce massive amounts of antibodies and secrete those antibodies into the blood. B cell encounters, the appropriate B cell encounters, the appropriate antigen, you see this B cell can't bind that antigen, so it's not going to be activated and, then the B cell has an interaction with the helper T cell which causes it to become the basic idea behind how these B cells are going to do their job. With that, let's flip the page.

Primary and Secondary Immunity

Antibodies can affect pathogens in a variety of different ways. One of which is called opsonization, 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 pathogen, makes it easier for the phagocytes to come over, identify, and then digest those particular pathogens. Now, antibodies can also neutralize and coat its exterior to the point where it basically can't function anymore. It can't infect a host cell because it's just covered in antibodies. It's like they form a shield around it, preventing it from interacting.

Agglutination, which is basically how antibodies can lead to clumping, occurs because antibodies, you might recall, are Y-shaped and they have two binding sites. Right? So, if one binding site 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 are kind of just stuck in this matrix of antibodies. This leads to clumping and rendering these pathogens neutralized, and you can see this clumping happening here and here on these particular samples. So, this anti-A, anti-B, anti-D, that's referring to types of antibodies and basically what's happening is the anti-A antibody is causing agglutination in this sample, and the anti-D antibody is causing agglutination in this sample but the anti-B isn't binding. There's no binding there so no agglutination. But you can actually see the clumping; it's pretty wild, right? Like these samples should look like this sample for anti-B but, you can see that the material which would give it that solid color all the way through is all clumped together.

Lastly, we talked about complement proteins and the innate immune system and I said that not only can these be activated by pathogen-associated molecular patterns but they can be activated by antibodies to create holes in the adaptive immune system and are 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 cytotoxic T cells which will be promoted by those Th1 cells. Remember, their job is to help activate those cytotoxic T cells and there's also the humoral response, which is 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 Th2 cells. So, those are basically the two aspects of the adaptive immune system.

Now, we have talked about what these effector cells do but remember there are also those memory cells being produced and their job is to deal with the secondary immune response. The primary immune response is what happens the first time you encounter an infection and 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 trying to identify and fight this infection. The secondary immune response is so much more powerful and potent. You see there's less of a lag in the secondary immune 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'd call active immunity where you get an infection and produce antibodies as 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 important 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've encountered while they are developing.

So, that's all I have for this page. Let's flip the page.

Immunization and Autoimmunity

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 specific defense against some pathogen. This usually happens through what's called vaccination. Vaccination is going to be the introduction of a vaccine to prime the immune system to deal with later infections. Basically, it allows you to mount a primary immune response to some weakened or killed form of pathogen that's not actually going to get you sick so that if you ever encounter, in the wild so to speak, that nasty bug in its form where it can actually get you sick, you have a secondary immune response ready to go to beat it down. Now, 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 'vacca', and essentially, if you're wondering why this has anything to do with cows, it's because the first famous case of vaccination in Western medicine, anyway, was with this guy right here. His name is Edward Jenner and he used the cowpox virus to vaccinate people against smallpox which was a rampant and deadly disease. And 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 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, a virus that's cultured in a species other than the host so it won't infect the host cells. This is not exactly an attenuated virus because, you know, cowpox is 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 are called subunit vaccines that contain isolated viral proteins so basically, some scientist will take a virus and break it down and find some good antigens to use and then, 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 biotechnology, you'll see things called monoclonal antibodies used and these are just antibodies that are prepared from a single clone of B cells, specific for some epitope. And these will be used often in research, for many different purposes, but you probably will see that name come up. Now, you'll know what it is. Now, things can go wrong with the immune system. Allergies are a common example of an abnormal immune response to an antigen which we'll 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. That's why, for example, if you're allergic to cats or something, the cat dander will make you sneezy. You can get that inflammatory response. Right? You'll get all swollen and puffy. It's just your immune system going a little overboard. Right? Identifying something as a threat that's not actually a threat. Now, allergies are unpleasant but they're not nearly as dangerous as autoimmunity, which is when an 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, in diabetes mellitus, it can be caused by an autoimmune reaction that has the immune system specifically target and kill the cells that produce insulin. And that's why, people with that condition can't produce insulin even though they have a pancreas because their immune system 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 CD4+ T cells and macrophages and this is obviously very dangerous because it's a virus that actually targets and attacks the adaptive immune system which is really bad news because it essentially can prevent your immune system from being able to mount an immune response not only against it but other pathogens as well. Those helper T cells, which are the CD4+ T cells, are needed for both the humoral response and the cell-mediated response. Remember, they're going to help activate cytotoxic T cells and they're going to help activate B cells to produce antibodies. So, basically, this virus attacks, 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 it's not a separate disease. It's a severe weakening of the immune system from an HIV infection. If you have an HIV infection, 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 sort of how HIV is a lethal disease is it just takes out your immune system so that even like a little cold or something could be fatal. Here, not to end on too dark a note, but here you can see a cell being attacked by HIV virus. So, with that, that's all I have for this lesson. Stay healthy guys. But if you get sick, now you know what your body's doing to fight against it.

Here’s what students ask on this topic:

What are the main components of the adaptive immune system?

The main components of the adaptive immune system are B cells and T cells, which are types of lymphocytes. B cells are responsible for producing antibodies that bind to specific antigens, while T cells require antigen presentation via major histocompatibility complex (MHC) proteins. There are two main types of T cells: CD4+ T cells, which become helper T cells, and CD8+ T cells, which become cytotoxic T cells. The adaptive immune system also includes memory cells that provide long-term immunity by remembering past infections and responding more rapidly upon re-exposure to the same pathogen.

How do B cells and T cells differ in their roles within the adaptive immune system?

B cells and T cells have distinct roles within the adaptive immune system. B cells are primarily responsible for producing antibodies that bind to specific antigens, neutralizing pathogens, and facilitating their removal by phagocytes. They can recognize free-floating antigens directly. T cells, on the other hand, require antigen presentation by MHC proteins. CD4+ T cells, or helper T cells, assist in activating other immune cells, including B cells and cytotoxic T cells, by secreting cytokines. CD8+ T cells, or cytotoxic T cells, directly kill infected cells by inducing apoptosis. Both B cells and T cells can form memory cells for long-term immunity.

What is the significance of antigen presentation in the adaptive immune system?

Antigen presentation is crucial in the adaptive immune system as it allows T cells to recognize and respond to pathogens. This process involves major histocompatibility complex (MHC) proteins displaying antigen fragments on the surface of cells. MHC class I proteins present antigens from intracellular pathogens to CD8+ T cells, leading to the activation of cytotoxic T cells. MHC class II proteins present antigens from extracellular pathogens to CD4+ T cells, resulting in the activation of helper T cells. This interaction is essential for the activation and clonal expansion of T cells, enabling a targeted and effective immune response.

How does the adaptive immune system distinguish between self and non-self molecules?

The adaptive immune system distinguishes between self and non-self molecules through a process called self-tolerance. During the maturation of B and T cells, those with receptors that bind to self-antigens are typically destroyed or deactivated. This ensures that the immune system does not mount an attack against the body's own cells. Additionally, regulatory mechanisms, such as regulatory T cells, help maintain self-tolerance and prevent autoimmunity. This ability to recognize and ignore self-molecules while targeting non-self molecules is essential for preventing autoimmune diseases and ensuring effective pathogen defense.

What is the role of memory cells in the adaptive immune system?

Memory cells play a critical role in the adaptive immune system by providing long-term immunity. These cells are formed during the initial immune response to a pathogen and persist in the body for years. Memory B cells and T cells can quickly recognize and respond to previously encountered antigens, leading to a faster and more robust immune response upon re-exposure. This secondary immune response is more efficient and often prevents reinfection or reduces the severity of the disease. Memory cells are the basis for the effectiveness of vaccines, which prime the immune system to recognize specific pathogens.