Understanding Adaptive Immune Response Components

Okay, so let's talk a little bit more about the components of the adaptive immune response. So if we're talking about adaptive immune system, there's three main types of cells. So we have two types of lymphocytes, our B lymphocytes or B cells that are going to oversee the humoral immunity. And then we have our T lymphocytes or T cells. So these are non-antibody producing lymphocytes, but they're going to constitute the cellular arm of the adaptive immunity. Our third cell type are what we call APCs or antigen presenting cells. They don't respond to specific antigens like our two lymphocytes do, but they do play a huge role. So T cells are T lymphocytes. They cannot recognize their antigens without... antigen-presenting cells. So we have to have APC cells in order for T lymphocytes to function correctly. So let's talk a little bit more about our lymphocytes. They are different, our B and T lymphocytes, but they do share a common pattern of development and some common steps in their life cycle. So if we're talking about the five general steps, the first one would be origin. So both lymphocytes originate in red bone marrow. The next step would be maturation. So where are they actually going to mature at? If we're talking about B lymphocytes, they're going to mature in the bone marrow. If we're talking about T lymphocytes, they're going to mature in the bone marrow. going to mature in the thymus. But lymphocytes, when we're talking about maturation, their education or maturation process takes about two to three days. And again, the location of their maturation is going to be different depending if we're talking about a B or a T lymphocytes. So why do we need to educate these lymphocytes? For two different reasons. One is immunocompetence and the other one is self-tolerance. So if we're talking about immunocompetence, each lymphocyte has to be able to recognize its one specific antigen by binding to it. So the ability for it to bind and recognize this specific antigen is what we we call immunocompetence. When our B or T cells become immunocompetent, they're able to display a unique type of receptor on their surface. And this receptor is what's going to allow them to bind to that specific antigen. So once the receptors appear, the lymphocyte is what we say is committed to react with only that distinct antigenic determinant because all of the antigen on it are going to be exactly the same. So the receptors, if we're talking about our B lymphocytes, they're going to be the membrane bound antibodies. The receptors on the T cells, they're not antibodies, but they're kind of like a product or an antigen that has the same kind of function as the antibody on the surface. And second step is self-tolerance. So each of our B and T lymphocytes has to be unresponsive to our own. own antigens, so our self-antigens, so it doesn't start attacking our own body cells, and that's called self-tolerance. The third step is seeding secondary lymphoid organs and circulation. So our immunocompetent B and T cells, they have not yet been exposed to their antigen yet. So we call those cells naive. So we have naive B cells and naive T cells. And those are going to be exported from their primary lymphoid organs to go off to other places. So our secondary lymphoid organs, things like... like our lymph nodes, our spleen, where they're actually going to be able to encounter the antigens. Our lymphocytes, especially our T cells, they're constantly circulating throughout our body. So by circulating them, it's also going to help increase their chances of coming into contact with an antigen in other parts of the body. So the fourth step is going to be antigen encounter and activation. So the first encounter between our naive lymphocytes and the antigen usually takes place in our lymph node or spleen, but it can also happen in our secondary lymph node organs. So our immune cells in our lymph nodes are really in a great place where they're exposed to a variety of antigen. So we can pretty much pick up a bunch of different things there from all the nearby tissues. Once we have our antigen binding to our lymphocyte that has this specific receptor for it, the antigen then selects that lymphocyte for further development. And this development is what we call clonal selection. If we get the proper signals, the selected lymphocyte will then activate to complete its differentiation process, which is the next step. So proliferation and differentiation. Again, we have to be activated by binding to the antigen, the specific antigen. Once it binds to the antigen is when we consider it being activated. And that's going to cause the lymphocyte to rapidly divide and pretty much form multiple cells, exact copies of itself with the exact same antigen specificity. And we call these clones. Most of these clones are going to become effector cells. and the effector cells are the cells that are actually going to go in and help fight the infection themselves. But a couple of the cells that result from this division are going to be what we call memory cells, and they're going to be able to kind of stay and respond much, much faster if we ever encounter the same antigen again. So we have both B and T memory cells and something called effector T cells that are constantly circulating through our body. Let's talk a little bit more about antigen receptor diversity. So we have genes, again, in our DNA, not antigens, are going to be what determine which foreign substances the immune system will actually recognize. And there are a variety of immune cell receptors are the result of acquired genes. knowledge of microbes. So basically we have a predetermined genes within our DNA of kind of like a background of the microbes that we are likely going to encounter in our environment. So approximately 25,000. different genes code for up a billion different types of lymphocyte antigen receptors. So we have a huge variety of receptors. And what we do with those 25,000 different genes is we shuffle them around so we can make multiple and endless combinations. So the antigen only determines which existing T or B cells will proliferate. And if they do, they will mount an attack against it. So most immunocompetent cells actually stay idle and they're never actually exposed to the antigen that they're programmed for. So we make a billion different types of antigen receptors and again those gene segments are stuffled and combined in what we call somatic recombination. So a little bit more about the lymphocyte education during maturation process. So T cells cannot bind to an antigen unless an antigen is presented on that self MHC protein. So the process of the education and maturation is best understood in T cells. So that's kind of what we're going to explain here. But it's assumed the same thing kind of happens in B cells as well. So T cells, again, they're going to mature in the thymus. under negative and positive selection pressures or tests, we have what's called the positive selection process, and then we have the negative selection process. The positive selection process is when T cells capable of recognizing our self-MHC proteins, those that aren't, are destroyed by apoptosis. So positive selection, we know they can recognize self so that they don't market as foreign. They're good. Then we have the negative selection process, which prompts apoptosis of T cells that bind to self-antigens displayed by self-MHC. So this process is called clonal deletion and ensures self-tolerance. So pretty much the negative selection process makes sure that our T cells don't attack our own body cells. If they do, if they're able to pass this and they shouldn't, then we have some sort of autoimmune disorder going on. So only about 2% of the T cells actually survive this process to become immunocompetent and self-tolerant T cells. So what kind of cells can actually present antigens? We have three major types, dendritic cells, macrophages, and our B cells or B lymphocytes. So dendritic cells, you may have heard of dendritic cells. of these before when you study the integumentary system. Because they are found in a lot of connective tissues and the epidermis or your skin. And they pretty much act as mobile sentiles, sentinels of boundary tissues. And they're phagocytic. So they can phagocytize pathogens that are capable of entering the tissues from some sort of damage. And then they can enter our lymphatics to help present antigens to T-cells in the lymph node. Their most effective antigen presenter that we know. and the key link between the innate and adaptive immunity response. So they help initiate the adaptive immune response. The next type of APC is our macrophages, and these activate naive T cells just like our dendritic cells do. What do they do? They present the antigens to the T cells. Once they present the antigen, it's going to activate the C cell, but also further activate the macrophage. So once we have an activated macrophage, then it becomes a ferocious phagocytic killer. So pretty much it's going to go in and eat up everything. It's also going to help trigger the powerful inflammatory response and help recruit additional defenses that we need. Then we have B lymphocytes. These do not activate T cells. Instead, they're going to present their antigens to help assist their own activation, which we'll talk about later. Here's a table. I recommend kind of understanding what's going on here, kind of going through the difference of our B lymphocytes and our T lymphocytes, the type of immune response, whether or not antibodies are involved, and primary target. So one thing I didn't point out... previously is that if we're talking about B lymphocytes or antibodies, the primary target is going to be extracellular pathogens, so things that are outside of the cell. If we're talking about T lymphocytes, their primary target is going to be intracellular pathogens. would be things like viruses. The cytoregination is the same. They're both going to originate in red bone marrow. Our B lymphocytes stay in the red bone marrow to mature, while our T lymphocytes will move on to the thymus to undergo their maturation process. And then if we're talking about B lymphocytes, we only have one type of effector cell. That's our plasma cell that's eventually going to produce antibodies. If we're talking about T lymphocytes, we have three type of effector cells. We have cytotoxins. cytotoxic T cells, helper T cells, as well as regulatory C cells. In either case, both of these lymphocytes can form cells that are considered memory cells.

And then we have our T lymphocytes or T cells. So these are non-antibody producing lymphocytes, but they're going to constitute the cellular arm of the adaptive immunity. Our third cell type are what we call APCs or antigen presenting cells.

They don't respond to specific antigens like our two lymphocytes do, but they do play a huge role. So T cells are T lymphocytes. They cannot recognize their antigens without...

antigen-presenting cells. So we have to have APC cells in order for T lymphocytes to function correctly. So let's talk a little bit more about our lymphocytes. They are different, our B and T lymphocytes, but they do share a common pattern of development and some common steps in their life cycle. So if we're talking about the five general steps, the first one would be origin.

So both lymphocytes originate in red bone marrow. The next step would be maturation. So where are they actually going to mature at? If we're talking about B lymphocytes, they're going to mature in the bone marrow.

If we're talking about T lymphocytes, they're going to mature in the bone marrow. going to mature in the thymus. But lymphocytes, when we're talking about maturation, their education or maturation process takes about two to three days.

And again, the location of their maturation is going to be different depending if we're talking about a B or a T lymphocytes. So why do we need to educate these lymphocytes? For two different reasons. One is immunocompetence and the other one is self-tolerance. So if we're talking about immunocompetence, each lymphocyte has to be able to recognize its one specific antigen by binding to it.

So the ability for it to bind and recognize this specific antigen is what we we call immunocompetence. When our B or T cells become immunocompetent, they're able to display a unique type of receptor on their surface. And this receptor is what's going to allow them to bind to that specific antigen. So once the receptors appear, the lymphocyte is what we say is committed to react with only that distinct antigenic determinant because all of the antigen on it are going to be exactly the same. So the receptors, if we're talking about our B lymphocytes, they're going to be the membrane bound antibodies.

The receptors on the T cells, they're not antibodies, but they're kind of like a product or an antigen that has the same kind of function as the antibody on the surface. And second step is self-tolerance. So each of our B and T lymphocytes has to be unresponsive to our own.

own antigens, so our self-antigens, so it doesn't start attacking our own body cells, and that's called self-tolerance. The third step is seeding secondary lymphoid organs and circulation. So our immunocompetent B and T cells, they have not yet been exposed to their antigen yet. So we call those cells naive.

So we have naive B cells and naive T cells. And those are going to be exported from their primary lymphoid organs to go off to other places. So our secondary lymphoid organs, things like...

like our lymph nodes, our spleen, where they're actually going to be able to encounter the antigens. Our lymphocytes, especially our T cells, they're constantly circulating throughout our body. So by circulating them, it's also going to help increase their chances of coming into contact with an antigen in other parts of the body. So the fourth step is going to be antigen encounter and activation.

So the first encounter between our naive lymphocytes and the antigen usually takes place in our lymph node or spleen, but it can also happen in our secondary lymph node organs. So our immune cells in our lymph nodes are really in a great place where they're exposed to a variety of antigen. So we can pretty much pick up a bunch of different things there from all the nearby tissues.

Once we have our antigen binding to our lymphocyte that has this specific receptor for it, the antigen then selects that lymphocyte for further development. And this development is what we call clonal selection. If we get the proper signals, the selected lymphocyte will then activate to complete its differentiation process, which is the next step. So proliferation and differentiation. Again, we have to be activated by binding to the antigen, the specific antigen.

Once it binds to the antigen is when we consider it being activated. And that's going to cause the lymphocyte to rapidly divide and pretty much form multiple cells, exact copies of itself with the exact same antigen specificity. And we call these clones. Most of these clones are going to become effector cells. and the effector cells are the cells that are actually going to go in and help fight the infection themselves.

But a couple of the cells that result from this division are going to be what we call memory cells, and they're going to be able to kind of stay and respond much, much faster if we ever encounter the same antigen again. So we have both B and T memory cells and something called effector T cells that are constantly circulating through our body. Let's talk a little bit more about antigen receptor diversity.

So we have genes, again, in our DNA, not antigens, are going to be what determine which foreign substances the immune system will actually recognize. And there are a variety of immune cell receptors are the result of acquired genes. knowledge of microbes.

So basically we have a predetermined genes within our DNA of kind of like a background of the microbes that we are likely going to encounter in our environment. So approximately 25,000. different genes code for up a billion different types of lymphocyte antigen receptors. So we have a huge variety of receptors. And what we do with those 25,000 different genes is we shuffle them around so we can make multiple and endless combinations.

So the antigen only determines which existing T or B cells will proliferate. And if they do, they will mount an attack against it. So most immunocompetent cells actually stay idle and they're never actually exposed to the antigen that they're programmed for. So we make a billion different types of antigen receptors and again those gene segments are stuffled and combined in what we call somatic recombination. So a little bit more about the lymphocyte education during maturation process.

So T cells cannot bind to an antigen unless an antigen is presented on that self MHC protein. So the process of the education and maturation is best understood in T cells. So that's kind of what we're going to explain here. But it's assumed the same thing kind of happens in B cells as well. So T cells, again, they're going to mature in the thymus.

under negative and positive selection pressures or tests, we have what's called the positive selection process, and then we have the negative selection process. The positive selection process is when T cells capable of recognizing our self-MHC proteins, those that aren't, are destroyed by apoptosis. So positive selection, we know they can recognize self so that they don't market as foreign. They're good.

Then we have the negative selection process, which prompts apoptosis of T cells that bind to self-antigens displayed by self-MHC. So this process is called clonal deletion and ensures self-tolerance. So pretty much the negative selection process makes sure that our T cells don't attack our own body cells. If they do, if they're able to pass this and they shouldn't, then we have some sort of autoimmune disorder going on. So only about 2% of the T cells actually survive this process to become immunocompetent and self-tolerant T cells.

So what kind of cells can actually present antigens? We have three major types, dendritic cells, macrophages, and our B cells or B lymphocytes. So dendritic cells, you may have heard of dendritic cells. of these before when you study the integumentary system. Because they are found in a lot of connective tissues and the epidermis or your skin.

And they pretty much act as mobile sentiles, sentinels of boundary tissues. And they're phagocytic. So they can phagocytize pathogens that are capable of entering the tissues from some sort of damage.

And then they can enter our lymphatics to help present antigens to T-cells in the lymph node. Their most effective antigen presenter that we know. and the key link between the innate and adaptive immunity response. So they help initiate the adaptive immune response. The next type of APC is our macrophages, and these activate naive T cells just like our dendritic cells do.

What do they do? They present the antigens to the T cells. Once they present the antigen, it's going to activate the C cell, but also further activate the macrophage. So once we have an activated macrophage, then it becomes a ferocious phagocytic killer.

So pretty much it's going to go in and eat up everything. It's also going to help trigger the powerful inflammatory response and help recruit additional defenses that we need. Then we have B lymphocytes.

These do not activate T cells. Instead, they're going to present their antigens to help assist their own activation, which we'll talk about later. Here's a table. I recommend kind of understanding what's going on here, kind of going through the difference of our B lymphocytes and our T lymphocytes, the type of immune response, whether or not antibodies are involved, and primary target. So one thing I didn't point out...

previously is that if we're talking about B lymphocytes or antibodies, the primary target is going to be extracellular pathogens, so things that are outside of the cell. If we're talking about T lymphocytes, their primary target is going to be intracellular pathogens. would be things like viruses. The cytoregination is the same.

They're both going to originate in red bone marrow. Our B lymphocytes stay in the red bone marrow to mature, while our T lymphocytes will move on to the thymus to undergo their maturation process. And then if we're talking about B lymphocytes, we only have one type of effector cell.

That's our plasma cell that's eventually going to produce antibodies. If we're talking about T lymphocytes, we have three type of effector cells. We have cytotoxins.

cytotoxic T cells, helper T cells, as well as regulatory C cells. In either case, both of these lymphocytes can form cells that are considered memory cells.

Transcript for:Understanding Adaptive Immune Response Components

Transcript for:
Understanding Adaptive Immune Response Components