Loading
Notes
Study Reminders
Support
Text Version

Effector Mechanisms

Set your study reminders

We will email you at these times to remind you to study.
  • Monday

    -

    7am

    +

    Tuesday

    -

    7am

    +

    Wednesday

    -

    7am

    +

    Thursday

    -

    7am

    +

    Friday

    -

    7am

    +

    Saturday

    -

    7am

    +

    Sunday

    -

    7am

    +

Video 1: Functions of Antibodies
Welcome back and welcome back to the immunology lectures. So, uh, today it's a, the lecture 10 and, uh, we will be discussing about the. Effector pathways or the effector mechanisms in the immune system. So over the last, uh, four lectures, uh, we have, I have been discussing the different parts of the, in it and the adaptive immune systems and particularly the mechanisms in the unit system and in the adaptive system, uh, the cells of the inner system, the cells of the adaptive system. So, what we have seen is that the inept system, which is the first line of defense has some specialized cells to deal with an antigen or a pathogenic invasion. Like for example, the macrophages, the neutrophils, uh, the mast cells, the basophils. These are kind of, these are the part of the eNett, uh, machinery, which is employed when there is all, uh, when there is an pathogen invasion. So like for every battle. So it's the immune system. It's a battle against the foreign pathogens. Like some, every battle you need, uh, uh, you need the army. So the person who will fight. So those are the cells of the immune system. And at the same time you would need the weapons. So like the different weapons of the battle and the weapons of the battle are basically the effectors. So who are actually working for the immune system. So if you need to win the battle, then you have to have some effectors. Because the cells by themselves cannot perform the function. The cells are just the army men of the immune system. So it requires the effector molecules, some effector mechanisms by which this battle is won. True. Are those effector mechanisms or who are those effector molecules in the immune system? So like in the inner system and in the adaptive system, we have seen, we have discussed the different mechanisms, how the neutrophils, uh, they migrate to the location and then they try to engulf, uh, the pathogen, how the macrophage. In golf, the pathogen induces, uh phagocytosis and, uh, in the, and then this, uh, after the pathogen is being killed, uh, then, uh, it can also present the S the, the, the peptides, the process to peptides, to the adaptive system, and then the cells of the eruptive system, they are induced, or they're activated, and they do some things by which they basically. Kills or clears, uh, kills the pathogen or clears the infection or the invasion. So now what is this? Something, what this something they do. So that is the topic of today's discussion. That is the effector mechanisms. What are the different effector mechanisms that actually work for the immune system and leads to the winning of the battle? Or leads to leads the immune system to win the battle. So we will be telling very, very briefly about the different, uh, effector mechanisms and the effector molecules today. And because these effector molecules, uh, as, as we progress in our lectures, in the future lectures, we will be talking about these effector molecules and the effector mechanisms very often, frequently. So I will introduce you. Uh, very quickly to the different effector mechanisms and the effector molecules that are involved in mediating an immune response. So let us start from the Arab system again, where we left. So in the adaptive system, the adaptive system of the immunity, uh, immune system, that up to brunch can basically be subdivided into two. You know, that's a humeral branch and the cell-mediated branch. So these are the two main branches of the eruptive immune system, the humoral and cell-mediated, and we have kind of discussed what are the processes of activation of the cell-mediated immunity? The process of activation of the B cells and all these, uh, series of events that occur in that active immune system. We have discussed very briefly, Nope, this humoral immune system effectively, they produces it's the B cell mediated immunity, and it produces antibodies, you know, It produces antibodies and these antibodies know what these antibodies do. The antibodies by themselves. They cannot do, uh, any function. So they need to, they need to go to the location and then they can do some functions with help of other effector molecules. So what do these antibodies do? These antibodies can do at least three different functions. One they can neutralize. So neutralization, they can, opsonize a pathogen. So it's also called opsonization or they can lead to activation of compliments, compliment activation. So these are the three major functions that the antibodies do so they can either neutralize the pathogen depending on the different types of toxins that are produced by the pathogen, for example, the bacterias. So they go and bind and, and by that, but by that they can recognize the pathogen and induces killing of the pathogen and then they can opsonize so they can, uh, go and coat the surface of the pathogen. So. Coating the surface of the pathogen and assist in the process of, so the golds and goats, the surface of the pathogen, they recognize the pathogen surface coats, the pathogen surface, and then they can help in the process of phagocytosis and then you can also have compliment activation. So now this. Is something new. What I told his compliments, this compliments are one, one of the very, very important effector part of the immune system. They belong both to the humeral branch. Uh, the adaptive branch as well as to the inner system. So there can be complement activation, which is antibody dependent, compliment activation. There can be antibody independent compliment activation. We will discuss about the compliments in very details in our upcoming lectures, but for the time being. Let us know that the compliment activation is one of the important functions that has been carried out by the antibodies and co. So the compliment activation in turn can lead to two functions. It can also lead to two different functions. What are this one is optimization. Again, it can also lead to opsonization. So antibody and compliment, they together compliment proteins. So these, what are this compliment is a compliment. Proteins are primarily small proteins or glycoproteins, which are being secreted from, uh, mainly the liver. And, uh, they are kind of proteases, which are activated and there is a cascade of activation events that occurs leading to cleavage of these complement proteins. So these compliment proteins, they get cliff, they themselves are not active. So the compliment proteins are named like C1, C2, C3, C4, likewise. See for compliment here. So they were, they are named, named as like C1, C2, C3, C4. And then once they are cleaved, they can form, uh, like C two, if it is cleaved, it can form C to a C to B. So like this, uh, three can be cleaved into C3 and C3 B. So this kind of cleavage is awkward and the compliment proteins, they get clipped into smaller, uh, proteins or peptides. And these actually assist. In the process of the killing of the cells. So the cells can be killed by the compliments by two ways. One is biopsy position. The other way is by license of the cell. So they can also Lise the cells by formation of the membrane attack, complex, something which is known as the memory Neta complex, or also known as Mac. So, uh, this is what the compliment proteins can do or upon compliment activation and compliment activation can be dependent on the antibodies. It can also be antibody independent. It can be antibody dependent, it can be antibody independent. So it can, uh, be a result of, um, uh, recognition of the various oligosaccharides. Uh, mannose that is present on the surface of the pathogen is being recognized by some other, uh, compliment proteins. And that can also lead to compliment activation, which is actually the Well antibody independent pathway and the antibody dependent pathway depends on binding of the antibody and recognition of the antigen. And that leads to the cascade of events, uh, follows a cascade of events that leads to the cleavage of different, different compliment proteins. Like C2, C3, C4, C5. And there is a long list. So we are not going to discuss it in details now, uh, because we have, uh, lectures, uh, designated lectures for that. So we will discuss there. So just for the timing, we, we just need to know that the antibodies by themselves alone cannot function. So they cannot do. Much, they also require some other effector molecules. They also require some other effectors, some receptors that some S some kind of receptors or some kinds of proteins that help them to opsonize or kill the target cells or the target pathogen. So this has to be very clear. And one of such effector mechanism is activation of the compliments or compliment activation. And one of such effector molecule is the compliment proteins. So. We got to know about the compliment proteins and the compliment proteins they can do again, they can do two types of function, precisely. They can do three types of functions, one they can do opsonization. They can lead to license by formation of the membrane Neta complex. What they can also do is they can enhance inflammation in hence the inflammatory risks. So. How, and, uh, in enhancement of inflammation, if you remember, uh, from our previous lecture on, uh, inflammation and the migration of the neutrophils, all these, uh, events, then it will very easily recollect that, uh, I told them. No regarding the cleavage products of the compliments. So there are compliments products like C three , which are also kind of, um, chemoattractants they work as chemoattractants, they're also known as sometimes they're also known as the NFL toxins. So they also help in enhancement of, uh, inflammation or inflammatory responses. So this is another part. This is another thing. So primarily the compliment proteins activation of the compliment proteins can lead to opsonization or lysis of the cell by formation of what we call is the membrane at a complex now coming to the cell-mediated part. So what does the cell-mediated part, the cell-mediated part can again, be broadly classified into two different, uh, parts, one we know is the. For the CD four CD eight plus cells, which finally develop into the cytotoxic T-cells. So the cytotoxic DC and the city four plus cells, which developed into dirty helper cells. Now this T helper cell or the T cytotoxic cell, they also help in elimination of the infection or the pathogen. Now, how so? The cytotoxic T-cells as the name suggests the cells themselves, they are cytotoxic, so they can go and directly interact with the cell. Which is infected. So for example, the infected cell or the infected macrophage, and it can kill that. So it can kill that cell, the target cell. So it has a target cell. It goes and kills the target cell directly kills the target cell directly. No. How, how does it do that?

Video 2: Role of Effector Molecules in Destroying Pathogens
So definitely there are some effectors or effector molecules that helps in this killing. By the cytotoxic T-cells and, uh, for example, there are effector molecules, which help in destroying the pathogens. For example, the grand designs, the granzymes and this granzymes are basically proteases so they are pro proteases. So, so the pro we use the term pro means they are not eat proteases. But they get transformed into active proteases when they are cleaved. So these granzymes are kind of inactive proteases and the, when they are released into the target cell, they become active proteases and they can, uh, do their functions with that. They can degrade the proteins and they can do a lot of functions. So this granzymes are released by the cytotoxic T-cells. And how do these granzymes they enter into the target cells. They enter into the target cells by the action of another kind of proteins, which are the perforins for example. So the perforins which assist in the entry of the granzymes. So that assists in the entry on the, of these granzymes into the target cell. So let us say, this is the target cell. And this target cell is then it is killed or apoptosis is induced in the cells, uh, by the action of the cytotoxic T-cells. And some of the, uh, important mediators of, uh, this cytotoxicity is for example, the perforins, the granzymes and also you have the fast ligand, the fast L. The fast Hill, which recognizes the fast. So this has been expressed on the surface. And then if it is recognize the fast, which is recognized on the target cell, and then it leads to apoptosis or the target cell. So these are all, uh, effector molecules that are being released or expressed by the cytotoxic T-cells, which helps in. Uh, recognition and killing off a target cell by apoptosis, you will be, uh, learning about this in more details, uh, from our later lectures for the time being, we are just trying to understand the different effector mechanisms that works in the whole immune pathway. So now again, so the, the weapons, basically these are the weapons of the immune system. So, and then we come to the T helper cells. Now the T helper cells, as I described, when I started talking about the adaptive immune system, the development and the activation of the T-cells, then I have two old already that the T helper cells, when they, the CD four plus interaction occurs with the class two, we made some molecules during the peptides of foreign peptides. I have shown this interaction in the last class. If you remember. So, uh, when this interaction occurs, then the CD four plus cells, they tend to differentiate into certain, uh, cell subtypes. And these are the, these are the effectors. So either they become the memory cells. Or they become the effector cells. The effector cells means the ones who will directly in the will be directly present in the Battlefront. So they will fight the battle. So they are the effector cells and they are effector cells by because they has the ability to, to somehow release something or produce something that. Kills the cell that kills the target cell. As for example, we have seen for the CDA plus cells. So there's T helper cells. They also are called Dobbs. Uh, the effectors subset of these TDD helpers includes the T H one. Do you help her one? And as I also told you previously, that is T helper cells are the city four plus cells. They differentiate into the different subtypes, depending on the availability of the cytokines now comes the name and other Victor molecule in the immune system. A very important one, the cytokine. Yes. So we will be discussing about the cytokines in future lectures in very, very details. I'll be teaching you about the cytokines later on, but for the time being, let us understand that the cytokines. They have a big role in, um, the effector mechanisms of the immune system and the cytokines are released by most of the cells of the immune system. They are released by most immune cells, immune cells by the lymphocytes and all other cells up by the path by the macrophages activated macrophages. They also release a lot of cytokines. So cytokines are one of the very, very, very important, uh, effectors. Effector molecules of the immune system. So depending on the cytokines, what cytokine is present in the surrounding that actually decides which type of subsidy of, uh, the T helper cell will actually be produced. So the T T cells, they, the T helper cells, there can be, uh, at least five different T helper. Cell subtypes have been identified. And this includes the th one, the th two th 17, the T reg or the regulatory T cells and the follicular helper T cells, the T F H I have told you in, uh, one of my last lectures about this five subtypes. No. But what do they do actually? So what functions do they do? So for example, the th one cells, they are involved in activation of the macrophages. They activate the macrophages, the activates, the. Macrophages and leads to the killing of the pathogen that is already there. So they activate the macrophages and leads to the killing of the bacteria or whatever it is present the th two type cells, the type two, the th two cells. They also do a lot of functions. So one of the major functions is, uh, of course, to, uh, help. The B-cell maturation, uh, sorry. Uh, the B-cell activation and in the class, switching of the antibody type. So this has a major role in class switching of the antibodies, um, in, in the, uh, during the process of B-cell differentiation and then the, uh, and mainly they they're responsible for product of IgE immunoglobulin, E you will learn about the IgE. Uh, when we, we were talking about, uh, Um, hypersensitivity reactions later on. So, uh, I, they can, they, they help in production of IgE, leading to, they can also help in the class switching of the antibodies on the B cells and the T helper cells. They also activate, uh, the, your cinephiles, your cinephiles and basophils. The cells of the immune system. They also help in the illusion of Hills basophils, um, uh, and, uh, killing of different other types of, uh, bacterials and pathogens. The th 17 is one of the important T helper cells that are essential for. Enhancement of inflammation. So one of the major functions of the TA 17 is to induce the epithelial cells to produce another subset of cytokines known as the chemokine lines. So they induce the epithelial cells mainly, and which leads to production of the chemokine. Give him all kinds of also produced by many other cell types as well. And so chemokine kinds. Are basically the chemo attractants, uh, earlier as well. What the chemokine SAR we have come across the chemokine, uh, particularly in the inflammatory response when we have discussed about the inflammatory responses. So chemokine ones are also are very important class of cytokines. They belong to the cytokine group family, uh, but they are mainly responsible for chemo attraction. So, uh, attracting cells from one zone to another zone. So cytokines are responsible for cell to cell communication and chemo kines are primarily responsible for cell migration. So that is why they are known as the chemokine because they are the chemo attractants and helps in chemo, Texas of the cell. So they help helping movement or migration of the cells. So this, uh, th 17 cells, they primarily synthesize the chemo kines and this chemo kines are, uh, responsible. As I told, they are responsible for the attraction of different leukocytes and primarily, uh, attracting more leukocytes, more neutrophils into the, uh, area of infection or the affected areas. So, and then we have the T reg or the regulatory T cells. And the T reg cells are primarily they're regulates the T-cell responses. So they basically, they are, they suppress the T cell response. And thereby they are usually the cells, which prevents the development of the auto-immunity. We'll be talking about the auto-immunity, uh, in, uh, India later lectures in the later part of this course. Uh, but for the time being, uh, so, uh, these T reg cells are one of the important cells, which regulates or the T-cell response, and primarily they're inhibitory, they has an inhibitory role. So that they suppressed the T-cell responses and the T follicular helper cells, as we have, uh, discussed earlier as well, they are important in the B-cell, uh, development and the class switching of the antibodies they are helping. And so they help in the B-cell development. In, primarily in this, uh, follicles in the, uh, uh, Domino's centers. So they are responsible for the B-cell development, the class switching, the affinity, maturation, all these processes, these TFH cells are responsible. No, let us quickly look into that as I told. So these are the effector cells and the effector mechanisms Wildridge. Hmm, the whole subset of the T-cells they work

Video 3: Effector Molecules of T-Cells
Now, let us quickly look into what effector molecules these T-cells they produce, or that actually leads to these functions. So the th one cells, for example, they are the major producers of interferon gamma. We will learn about inf gamma signaling, uh, later. So they produce this interferon gamma and TNF alpha, which is. Too many crosses factor alpha th two cells, they produce interleukin four and interleukin five mostly, which are the major cytokines that are involved in, uh, uh, class switching of the B-cells the antibodies on the B-cells. And they also produces the GM CSF. With the granular side, macrophage colony stimulating factors, then the T eight 17. It produces interleukin 17 and also interleukin 22. So these are the interleukin. 17 is one of the major cytokines, which helps in activation of the epithelial cells and, uh, leading to the production of the cytokines or, uh, they, then they start producing the cytokines and aisle 22 has direct role in enhancement of inflammation. The TDX cells are primary producers of iron tin. And I attend is known to be one of the important interleukins are one of the most important cytokines that are involved in, uh, anti inflammatory responses. So it is basically also sometimes called an anti-inflammatory cytokine or interleukin. So I L 10 is released by the T reg cells as they are. The major cells, which are responsible for suppression of the T-cell responses. So these are some of the effector molecules that have been produced by this, uh, T-cell subtypes. Or the T cells, the T helper cells that mediate that actually mediate the function. So these are basically we can, where we can draw an analogy and we can say these are the bullets basically, which are being, uh, thrown by the immune system and the cells are the warriors, or they are the army men. Of the immune system. And then you have more effector molecules if we, so this, these are the primary effector molecules that are involved mostly in the adaptive part of the immunity as full as in the enact part, we also get, uh, in the cytokines are everywhere. Remember? So the cytokines, they are, uh, almost everywhere and in the innate part. So the, in the in system. So like we have the adaptive system and we have the inner system. So in the unit system of the, uh, uh, immune branch, they, uh, of the immune system, uh, we also have different types of cytokines and they are primarily produced. By an activated macrophage. So an activated microphones, which has engulfed a pathogen, for example. So this is an activated macrophage, which has, uh, phagocytosed a pathogen can also produce different types of cytokines. And which is also the effector molecule, so they can produce many cytokines, like the interleukin six, the TNF alpha interleukin one I'll one, for example, interleukin one B I L six. TNF alpha. They can produce a lot of these effector molecules that does a lot of different functions in the innate part of the immune system, apart from the cytokine. So you can see that the cytokines has a big, big role in. Both the additive and the immune system in the communication, the cell cell communication in other very important thing is the chemokine. The chemokine has a big role in cell attraction or cell migration, so they can attract the, uh, different cells, uh, to different locations. For example, um, the dendritic cells. So the dendritic cells are licensed to go to the lymph node. And, uh, for that, if the process is called the licensing of the dendritic cell and their chemokine is, has to play a very important role. So chemokine is they go and bind to the chemokine receptors. So some cells. They express the chemokine receptor on their surface and some cells that produce the chemokine. So when there is chemokine in the surrounding that that will go and bind to the receptors and that will, uh, attract those cells, uh, towards that location. So that's how the signaling soccer, so the chemo kinds or the chemoattractants, which attracts the cells expressing the chemokine receptors. So the, and the cytokines, as I described here very quickly, So it will be explained very, very level directly in our, in my letter later lectures about, uh, we will be talking yeah. About the cytokines, but for the time being, we get to know that cytokines are one of the major key players in the whole, in the effector mechanisms of the immune system. So cytokines are involved in the, in it pathways as well. And as I told the compliments are also present in the unit in a unit system, as well as there are other effector molecules. I have told, like, for example, uh, we have the, the histamines, the histamines histamine, the prostoglandins. and the leukotrienes. So these are also present, and these are primarily, these are also part of the immune effector pathways, uh, the, uh, primarily the internet, the enact pathway, and these are also, uh, they, what function they do is they increases. They increases the vascular, the vascular permeability, and they also, uh, lead to smooth muscle contraction. So these are also kind of the effector molecules of the immune system that are mostly involved in the eNett. Pathway. So if you look into the whole picture, the different, uh, effector mechanisms and the effector, uh, molecules of the S of the immune system, we have identified among them are the compliment proteins. Then we have, of course, the antibodies, the compliments, the different types of small molecules, enzymes, like granzymes, perforins. And then we have the cytokines. We have the chemokine lines, different cytokines, different types of cytokines. We have histamine, we have the prostoglandins, the histamines, which are mostly, uh, enhancers of the inflammation. So they are involved in inflammatory responses. And also we have these cleavage products of the. Um, compliment pathway or the complement activation pathway. So all of these molecules, these effector molecules, they work together to enhance. Or to amplify the signal. So they are the effector molecules that actually effectively work on, uh, the different target cells and tries to kill the different target cells. So, uh, we will be talking, uh, more elaborately or we will more discussed more and more about this effector molecules, the pathways that are involved, effector pathways, uh, in our upcoming lectures. Uh, so, uh, this much before today, it's this much and we end, uh, the lecture here. Thank you very much.