[Music] in this video we're looking at an overview of the whole of the main response that we have in our body so in Chapter 12 which is all about the communicable diseases I've spent a couple of different videos talking about the separate parts of an immune response so we've got the nonspecific ones and the specific ones as well and we've got different types of nonspecific and specific responses and in this video I thought it would be quite good at if we just kind of summarize everything and just pull everything together to look and see how the entire body works together to to make sure we fully understand the entire full complete immune response right so actually the immune response is kind of like a story and it's got four different parts to it so it got inflammation as the first step then phagocytosis then the specific ones cell mediated and humoral responses and obviously with on the afterwards which is about how do we stop the whole immune response which I'll also talk about here in a second so we're going to first of all start at the first stage so in the beginning remember we've got the physical defenses or our primary defenses which are kind of like our skin the sebum on the surface of our skin mucus in our Airways and if we have wound we've got the scab over it and also if it's enough food then we got the acid in our stomach to actually killed these pathogens so we got the physical primary defenses however if the pathogens manage to get through these physical defenses and get into our bloodstream into our actual body system then the first thing happens which is inflammation right so when the infection started first of all there's a type of cell that is activated which are mast cells so this little symbol here sends forth activation so and muscles are activated and they release two different chemicals which are histamines and cytokines right there are two major effects of histamine and both of which are also affect the blood vessels they make the dilated blood vessels and also they can make the blood vessels more leaky so the walls are more permeable and because of these two effects they can to show the four different symptoms of inflammation because of the dilation of the blood vessels or you can call vasodilation it would lead to two specific symptoms localized heat and redness so the point of having a localized heat actually is by increasing the temperature pathogens of reproduction rate boots slowed down but they just naturally don't like to be in a really warm temperature and the retina surface they just shows that because dilating the blood vessels would mean that more blood is flowing to the surface of the skin therefore it shows a sort of a red patch on our skin and the point of that is actually by bringing more blood to those infected areas in the inflamed area then we the ideas about making the blood vessels more leaky and so that we can make more tissue fluid right and the idea is that because they're more likely some of the other molecules can also come out that naturally stay in a flat shape so for example y+ cells is the main one all right so the white blood cells are normally quite big so they can't screw through and also we'll talk about in terms of phagocytosis there are specific what forces that can go out and some that stains in there but the idea is that you increase tissue fluid so you're bringing more of the chemicals to that inflamed area so that they can tackle it and the two symptoms here will be swelling and pain because obviously if you've got mortage fluid there it's squishing onto the pain receptors obviously then you feel the pain and also the swelling is because you got more fluids there and then on the other hand we got the cytokines right which actually attracts phagocytes and obviously because they track phagocytes that's why we say that they will lead to the second stage which is phagocytosis so we'll talk a bit more about that now now actually there are two types of phagocytes right remember that anything that ends with SI y te usually is talking about a cell and we've got two different types of phagocytes both of which do phagocytosis one of them is called neutrophil and the other one is called macrophage and they have distinctive structural differences between them even though they pretty much do the same thing so on the left hand side we've got the neutrophil on the right hand side we got the macrophage as you can see from the picture there are a couple differences number one is the nucleus so neutrophils have a loathed nucleus and macrophages have a larger round nucleus and what that means is that the neutrophils are able to squeeze through the gaps in the blood vessels to leave the blood vessel so when we talk when we talk about histamines making the blood vessels more leaky actually it's about making more neutrophils leave the blood stream to directly and gulf the pathogens at the infected tissues whereas macrophages mainly stay in the bloodstream but the thing is they have a very very important function right so the other thing is you will notice that both of them have one thing in common to restructure which is the lies of lysosomes right so both of them have Lices are in there and the lysosome is basically a specialized vehicle that contains enzymes like various hydrolytic enzymes which we just call lysozymes but actually Eliza limes is just talked about the group of enzymes which are protease is lipases and carbohydrates because we know all pathogens for all living cells or living beings are just made up of proteins lipids and carbohydrates so lysozymes hydrolytic enzymes are literally just a mixture of all of those enzymes so both of them have that one then the other thing that the macrophage has but the neutrophil doesn't is that they've got the MHC which is the major histocompatibility complex right so the neutrophil doesn't have them but then the macrophage does because the idea is that the MHC the major histocompatibility complex is a protein that can turn the macrophage into an antigen presenting cell to alert the rest of the body about theme about this invasion of the pathogen where's neutrophil literally just DeFalco cytosis they don't do anything else they just literally digest and golf digest the pathogen and that's it that's why the neutrophils can actually digest if you know a pathogen in about ten minutes was the macrophage will take a little bit longer because it's not just there jesting the pathogen but also keeping the antigen and then prison so we look in the actual process of that of how macrophages does this as follows so in the beginning this is the engulfment of it so we say actually this is the pathogen and we've got some antigens on the surface of it sometimes these pathogens can be tagged by chemicals called obstinance and these obstinance are actually antibodies and what they do is literally tagging the pathogen and making it a little bit more obvious for the macrophages to mop them up so rather than just have it's almost like playing Heinz hide-and-seek in the dark so if you're if you can imagine if you've got a gun with some sort of fluorescent dye and glow-in-the-dark paint on it and you can shoot around and anyone you're trying to catch will you know be painted with that blown adult paints so it makes it easier for you to catch them same way in this case the pathogens can be tagged by the obstinance making them more obvious to the macrophages to engulf them so this is the case so they extend their cell membrane and their cytoskeleton to engulf the pathogen make sure you use the word and golf and not eat because they do not eat things they don't have a digestive system they engulf the pathogen and then the pathogen inside will turn into the vesicle that contains the pathogen will be called a phagosome all right anything that ends with s ome is pretty much a physical and we got the lysosome here as we mentioned earlier and then these two physicals will then fuse together and then we've got this big particular vesicle which we then called a Fraggle lysosome and I think that's kind of is why because it's just a fact or some analyzer on attack combining together making a of a schism then we've got the MHC here which we mentioned earlier and then finally the lysozymes would digest the pathogen except for the antigens and then the antigens will be combined with the MHC to be placed onto the surface of the cell so here we've got the digested pathogen here and there are different ways the cell can actually release these digested chemicals out towards the outside or they actually change all of this into something useful for themselves because remembering that they're just a pathogen is literally things like amino acids glycerol fatty acids sugars simple sugars etc because that's what makes up the cell right so then the macrophage now becomes an antigen presenting cell and then they can then enter or signal the rest of the world about this particular invasion and then turning this whole response to a specific response because up until now the inflammation and the cytosis can literally be any pathogen and then it's at this point then they tell the body okay is this particular pathogen that is infecting you so therefore we need to try to make turn this response to be specifically towards that particular pathogen and this third stage is cell mediated response so the first thing is that the we've got different white blood cells here or we call them lymphocytes so we got the phagocytes which are the neutrophils and the macrophages and actually for the lymphocytes we've got so many different types there are two major families we've got the T lymphocytes and the B lymphocytes T lymphocytes they are made in the bone marrow but then they mature in the thymus that's why it's called T in it whereas B lymphocytes or made and mature in the bone marrow hence called the B cells so the first one will be the T helper cells and the reason why the T helper cells can do this is because they've got a very specific receptor as shown here and this receptor is called the cd4 receptor and the cd4 receptor is specifically going to recognize the antigen MHC complex here so they recognize the antigen MHC complex specifically and then that activates the T upper cell in order to do loads of different things one key thing it does is to release a very specific chemical actually it is a type of cytokines but then because it's by the t lymphocytes we call it the interleukins but keeping in mind cytokines are like a family so as mentioned earlier here silicones are a family of chemicals that are responsible for cell signaling so how for example here it can signal the phagocytes to engulf pathogens and in this case a specific type of cytokines which are interleukins released by T helper cells can signal other cells to do various different functions so first thing is by because of this activation it would trigger the T helper cells to start dividing by mitosis and also specializing into various different other types of cells so first of all it can make T memory cells which will be responsible for the immunological memory for a second response we'll come back to this later they can also make T killer cells and as the name implies they killed the cells and they do that by releasing two different chemicals so the first of all they're released as a chemical called perform which basically punches holes into the cell or oil the pathogen so it could be a pathogen itself or it could be a viral infected cell or even a cancer cell right so they just recognize that cell being being infected or not self has not got a self antigen bug or foreign antigen they release a preference to punch the holes in the cell membrane making the cell lose its integrity so all the stuff inside comes oozing out and also they can release hydrogen peroxide which is a very toxic chemical and it kills the PAP kills the cell or pathogens directly so that that's the killer cells or sometimes you might have heard another name called cytotoxic T cells another T cell that they can make is T regulatory cell and they have a very specific function but it doesn't come we don't necessarily come back to this until later on because the idea is that the T regular cell actually suppresses the immune system so the idea is that it kills all of the other active white blood cells that was previously used to control everything and the idea is because if the rest of the these T cells are B cells get carried on after the infection is finished they actually going to overdrive and then that work they would start attacking our own body cells which is what we called autoimmunity so the idea is that they can prevent that from happening but we can come back to this mates arm so these are the three T cells that the T helper cells will then divide and differentiate into which helps with the body in terms of the immune response another thing that they can do is to actually signal the B cells to start working now it's probably worth mentioning that apart from the macrophages becoming an antigen presenting cell the B lymphocytes can also do the same thing so actually we can have something called the B antigen presenting cell and they similarly they can present how they can do phagocytosis and then present the antigen on the surface which is again recognized by the T helper cell with the cd4 receptor and the way that they chose which B cell can actually do this is determined by what kind of antibody they actually have and this is what we called clonal selection so for example here we've got various B cells alright or we call them B effector cells and they all have is like okay makes a slightly different antibody but as you can tell from the different shapes but the thing is if we if you pick a particular B cell that makes this particular shape of an antibody it which is not complementary to the coverage and then it wouldn't actually work so they need to find something that is complementary to the antigen you know for in order for the immune response to actually be useful so they're more response the fourth stage is about this basically split into two parts the first part is the clonal selection selecting the correct B cell that makes the correct antibody to be activated which then they then divide and further differentiate into different B so different types of B cells and this is what we call the clonal expansion and again remember it is by mitosis that they do that so there are different types of B cells that they can make namely actually two so one of them is the B memory cell which serves the same function here which is the immunological memory what that means that may be the first time the first time you've got infected then your body can make a little bit of antibody but then they very quickly get destroyed but then if afterwards after t-regulatory cells kills all of the other cells the memory cells will still stay in the system and they can recognize the pathogens the same pathogen if they infect again the next time and then they start making this trigger the whole response and they're very short on my time so they make they can make a lot more antibody in a very short amount of time and this is what we call the secondary response here and then some of the other B cells the B antigen presenting cell can actually divide by a clonal expansion into more B plasma cells and the plasma cells are responsible for making more B plasma cells which is what we call the clonal expansion and the idea is that you are making more of these cells that can make the same type of antibody so all of them make this antibody off this particular shape so we would say that they make a specific antibody which can then go on and target the antipode go on and talk of the pathogens and the rest of body to quickly wipe them up so what's important is actually think about what do these antibodies actually do in the structure of it so antibodies can also be called immunoglobulins which are a family of proteins that specifically recognizes antigens right so usually they have this particular Y shape you should know that they are made up of different chains we got the heavy chains which is kind of the inside bit and then the light chains which are the two chains on the outside here I've drawn it so guys it looks a bit like this but actually it should be two separate chains here and then two separate change that and they joined together in various places for example here by disulfide bridges and which obviously as you know from biochemistry the stuff where bridges are the strongest type of bond there is and that that's why it gives it a shape a structure and making sure it works and then we got different regions we got the variable regions on the ends of that so this part here can actually change depending on the type of antigens that you're meeting so a lot of people think thought that the antigen will bind in the middle here that's because because that's how we often draw it in in the simplistic term but actually that's not the case they can join each antibody here can actually join to two different antigens at that very end there but usually in the other case which we should you draw here for some sake of simplicity so that's the variable region and the rest of the antibody is the constant region you should know what the structure is and be able to label the rest of that as well right so the antibodies or the immunoglobulins actually have various different functions they can directly attack the pathogen itself these ones in the middle are representing those antibodies and then we got the pathogen at the different parts this is always saying that the antibodies are doing agglutination and we say that they are acting as agglutinins what they do is actually as the name implies they're gluing the different pathogens together and what that happen what they do is that it makes the entire batch of them a lot bigger so that it's easier for the macrophages or the neutrophils to come and mop them up by phagocytosis is literally about making their batch baker again using the same analogy imagine if you're playing hide-and-seek then all of the antibodies it's like you're shooting and you've got a glue gun this time and you're shooting out glue and it stuck all of those people together so it's harder for them to say hide under the table or you know hide behind the curtains because they're so big so it's easy for you to catch them so it's about making the pathogen stuck together then another thing here is one single pathogen but loads of antibodies around it we've already mentioned that earlier on is what we say that they can act as obstinance as well so by tagging a pathogen making them more obvious for phagocytosis another thing here is let's say we got bacteria and is releasing lots of toxins then these antibodies can directly attach the toxins and then render them useless or neutralize these toxins so we say that they can also act as antitoxins as well so these are four major functions of antibodies so imagine that they because of the V plasma cells rapidly producing all of these specific antibodies they which can do all of these different functions then very quickly the pathogen is wiped out that at the end will come back to this one we mentioned this before the T V regular cells kicks in so I'm going to simply say that this is going to be the end so to see regular cells then comes in kills all of the other pattern all of the other white blood cells except for the team and the cells and the B memory cells which we need to keep for the next time so they kill all of the other cells except these two to make sure that our immune system doesn't go into overdrive and start killing everything else so here we're going to do a quick run off the entire process so in the beginning you or let's say running outside you fell over and then you've got you started bleeding on your knee and some of the pathogens got into your system where some of the others were blocked by the physical defenses and the scab starts to form over your wound to stop further pathogen entry however some of them already got into your bloodstream so as saucers traveling around the body but some of them let's say underneath triggered an inflammation in that particular area so first thing happens is that the mass cells are activated by the entry of the pathogens and they release two chemicals histamines and cytokines histamines will dilate the blood vessels and make them more leaky as well which causes for which you will notice by the four different symptoms so it feels a bit warmer in that particular area which makes the pathogens harder to reproduce themselves it will also appear red because there's more blood flow into that this is a skin surface there's also two more tissue flow formation because of the permeability of the blood vessels therefore they're swelling and also pain that comes with this running and the idea is to make more neutrophils a becoming able to come out of the bloodstream to do phagocytosis on the other hand the cytokines are a family of chemicals that are responsible for cell signaling so they would track the phagocytes which then leads it on to our second stage which is phagocytosis so we've got two types we've got the neutrophils and macrophages as the phagocytes neutrophils can squeeze out and try and kill those pathogens on the fected areas but they cannot become an antigen-presenting cell however macrophages cannot leave the bloodstream so they cannot get to those infected areas however they will stay in the bloodstream and become an antigen presenting cell to alert the rest of body to have a specific immune response so they were engulf the pathogen which may be tagged by antibodies already then forming a phagosome inside the Faculty of no fuses with the lysosome to become a freckle lysosome and then the enzymes inside digests the rest of the Puffin except for the antigens which then bind with the MHC to become an antigen pretty complex which is then presented onto the surface of that macrophage then the matter that particular APC will be recognized by the T helper cell because it's got a cd4 receptor and this is what we call the cell mediated response the activated T helper cells can then to do different things it would release interleukins which can then signal more T helper cells to divide by mitosis and also recognize and b cells that have also done focus or ptosis become an aunt an antigen presenting cell triggering the humoral response which is the next part on the right here so let's talk about this one first then T helper cells can then divide and specialize intuitive regulatory selves t killer cells and t memory cells tickle cells actually release chemicals that kill the pathogens whereas timur cells would stay to provide immunological memory but recognizing the same pathogen the next time around then it can also the intelligence will also travel to the b cells here and triggering them to undergo clonal expansion and clonal selection and the first bit here so for the correct b cell is being selected due to their specific antibody and then clonal expansion will then happen making more b plasma cells and also some of them become b memory cells which can do the same thing as team and resolves then all of those b plasma cells will then mass-produce the antibody the specific antibody and they can then do four different things the antibodies or immunoglobulins can directly attack the pathogen or they can act as a gluttonous so that they can be engulfed by macrophages or the neutrophils easier they can tag the pathogen as well so they're acting as opsin instead or they can become anti toxins which render the toxins useless and then at the very end of it once most of all of the bacteria or viruses have been wiped out then T regulatory cells comes in kills all of those white blood cells and immune cells except for the memory cells and the idea is to suppress it so that it isn't going to overdrive becoming an autoimmune disease and then the team and missiles and B memory cells will stay around the bloodstream and if the next time we've got the same pathogen coming in again but live this time let's save the first time you've done all of this is because of a vaccination the sector second time it comes around it will recognize them very quickly skip the first two stages of the nonspecific responses and go straight into specific response by producing a lot of antibodies in a very short amount of time killing those pathogens before we actually start getting those symptoms and stop becoming sick and this is the overview of the immune response [Music]