all right ninja nerds so the goal of this video is to cover an entire adaptive in an innate overview and again I get a prize if I win if I do this under 20 minutes so we're definitely trying to make this kind of quick good overview here so again starting with innate immune system right with the innate there was some type of damage right because of this bacterial cell it caused the release of endotoxins caused what a massive release of inflammatory cytokines right such as all of these ones that we've already talked about here what
is the overall results of these guys one thing that they're gonna do is is they're gonna act on smooth muscle cells and cause vasodilation which increases the blood flow and causes heat and redness they're also gonna act on the endothelial cells cause contraction right which is gonna cause a lot of fluid to leak out increasing permeability and a lot of fluid leaking out can compress on the pain receptors and variety kinase can activate Prine pain receptors inducing pain and that fluid exudate that leaks out can cause swelling so that covers swelling pain heat and redness
which are the four cardinal signs of inflammation right and if there's a really really bad form of inflammation like you burn your hand to third-degree burn around your hand it actually can cause a lot of inflammation around this joint to where you can't move it right it's not your joint in mobility what else can happen these histamines and all these other chemicals they can also cause the production of certain types of cell adhesion molecules and we've already talked about these in great detail there's no need to go over them again these things could be like
pee selectins ISA lectins eye cams and v cams and what is their whole purpose to enhance the margination response in other words cling to the edge of the capillary bed and rolling on the surface right then as it rolls it can move through the actual endothelial cells by Dionysos which is that amoeboid motion and then what i can actually migrate to the site of injury where all these bacterial molecules are due to these inflammatory chemicals and it's gonna move towards that area by positive chemotaxis right so that's the overall result there what else can happen
though a lot of these inflammatory cytokines that's also being released like Lucan one to manic rhotic factor-alpha and her Lucan six what can they do let's follow it up here look what they can do they can cause fever within the hypothalamus right they can cause the liver to produce C reactive peptide which is a good indicator of active inflammation and they can trigger the bone marrow to make more leukocytes via leukocytosis that's the entire inflammatory response for the vascular and some of the cellular effects right so it's not that bad right now what else can
happen well once these phagocytes get out here into this area and they start fighting with this bacteria what can be the result phagocytosis they eat the bacteria right so they take the bacteria in through their pseudopods I'll just call phagocytosis and remember they form the phagosome combined with the lysosome form the lysosome break them down through the lysosomal action but neutrophils sometimes depend upon how intense the bacteria or form a microbe may be it might have to do free radical reactions called oxidative burst or release it's chromatin out into the extracellular space to tag bacterial
molecules for destruction from from like for example cut deep Sanji what else can happen the macrophages they can phagocytose those actual bacteria and actually what expose those antigens on the cell membrane with MHC 2 molecules major histocompatibility put complex type 2 but remember all nucleated cells all nucleated cells in your entire body expressed what's called MHC 1 molecules so that's important and we'll talk about when we get to adaptive all right so that's one mechanism there what else can happen remember you also have complement proteins your livers are constantly making these complement proteins and they're
circulating within our plasma in the inactive form and whenever they're in the inactive form what can happen whenever they actually act it they're become activated due to certain types of chemotaxis or due to the increased permeability or due to the FC portion of antibodies so on and so forth what happens you activate these proteins and they undergo specific Cascades like the classical pathway which is antibody mediated right so as to be antibody meated then it starts with c1 and it goes all the way to c9 producing c3 and c5 a which enhance inflammation alternative is
not antibody meted it's directly binding c3b with the foreign pathogen and that caused that whole process again right and then lectin you just need a man''ôs and electon binding Manos to trigger this entire cascade what's the overall effect of these these pathways right here to produce the membrane attack complex to initiate a lysis of the bacteria or to enhance opsonization by the c3b or to enhance the inflammatory response to c3 a and C 5 a so that's the complement system still in the innate now what else we also said what if we have these cells
here are macrophages are general tissue cells what if they're infected by a virus so they're infected by some type of viral molecules right if they're infected by the virus so this is these cells are infected by a virus what can happen they can activate genes to produce specific types of molecules called interferons like alpha beta and gamma what do alpha and beta do they activate what they come over here to a nearby healthy cell and tell those nearby healthy cells to produce antiviral peptides for example protein kinase r what does that do it actually destroys
the actual virus or prevents the virus from attaching right and prevents this virus from causing damage in these tissue cells what does gamma interferons do well the only one who really secrets gamma interferon is because we have them over here remember alpha and beta interferons are produced by tons of cells a lot of different cells beta interferons are usually specific to making platelets though a front they're made by platelets right Gami interference are made by specific types of cells like your natural killer cells your lymphocytes your macrophages what are those gamma interferons do we already
showed it over here right these gamma interferon x' is secreted by macrophages or natural killer cells or lymphocytes they come over activate other macrophages and then do what caused these macrophage to proliferate get bigger get hungrier and increase the expression of class 1 and class 2 molecules all designed to enhance the inflammatory response right then what else alpha and beta they can also cause the activation of natural killer cells who can come in and start killing some of these virus infected cells so it's a beautiful thing right and that is a part of our innate
immune system still now lasting for our need immune system we have these toll-like receptors in these toll-like receptors we have 11 different types right so many different types but there's 10 that we're only talked about here because we don't know the function of toll-like receptor 10 what is the overall result of all these because they're all responding to different types of pathogens the overall result is the production of specific types of signaling proteins for chemotaxis right or the production of interference like alpha beta and gamma interference and the production of tumor necrotic factor alpha interleukin-1
beta and interleukin 18 and remember these guys have to be acted on by caspases to become in their active form because then they're their preformed right now or their proform what do all these guys do they enhance the inflammatory response enhance chemotaxis and tried to be able to eliminate de foreign pathogens from the body right that's the desire now then we go into the adaptive immunity what was the adaptive effect you remember we took these macrophages with the MHC 2 molecules and we also took these free antigens and we take them into a lymph node
well what was the effect here so again what do we do we take this macrophage and we take these free antigens and we bring them aside lymph node right because we already went through the phagocytosis process and we know that the neutrophils exocytosed what those free antigens the macrophages are good antigen presenting cells those as well as lymphocytes and specifically antigen sorry dendritic cells they come in and what happens let's see if we follow the free antigens first the free antigens are the exhaustion as antigens bind onto a naive B lymphocyte activating that by a
B lymphocyte right that B lymphocyte then can bring in the receptor mediated endocytosis bring that antigen in and produce MHC 2 molecules against it right and expose it on the membrane surface but that activated lymphocyte which also has all these BCR receptors specific to that antigen he can't get stimulated to proliferate yet why because he needs some type of stimulation from other cells so what's those other cells remember the macrophage the macrophage is going to be coming over here it's having its MHC 2 and the foreign antigen it brings it to a naive T cell
T helper cell right that T helper cell will have cd4 positive proteins it will have a TCR our t-cell receptor Pacific to that foreign antigen which will interact when they interact it activates a cd3 molecule which sends this primary signal into the nucleus there also be Kiko stimulation signals between b7 and cd28 and then there also be the secretion of interleukin 1 what does this do interleukin 1 that third signal will activate this T helper cell to produce interleukin 2 and there also be the production of interleukin 4 from other cells which will bind onto
this actual T helper cell then what will happen whenever this interleukin 4 and interleukin 2 bind it triggers the T naive cell to start proliferating and becoming specialized and differentiating into its called th 2 lymphocytes because remember enter Lucan 4 converts the naive T cell into th two interleukin 12 converts the naive T cell into th 1 or T helper 1 cells so now our teach two cells are activated they're ready to start producing specific types of interleukins what are those interleukins one of them is interleukin 4 and our Lucan 5 and interleukin 6 and
then Lucan 4 is the very signal that these activated lymphocytes need to start proliferating what does that proliferation called it's called clonal expansion and you're making all these b-cells with the BCR specific to that foreign antigen that we've started with this whole process they expand interleukin 5 stimulates these actual activated B cells to undergo differentiation so again what does this step right here called this is actually differentiation so differentiation right here will convert these actual b-cells into memory cells or plasma cells memory cells will stay in our body for awhile right with that specific b-cell
receptor specific to any foreign antigen the plasma cells will respond to interleukin 5 and interleukin 6 and they'll produce antibodies and what will those antibodies do these antibodies what can either do a couple different things right we talked about it very briefly they can bind with these foreign antigens and cause the neutralization reactions precipitation reactions lysis and we also set agglutination reactions to right so there's a lot of different opsonization will go into more detail on those in antibodies right alright so again they can undergo the opsonization reactions right now that whole thing that we
talked about is humoral immunity what is humoral immunity it's the effect again one more time of those at exogenous antigens stimulating these actual b-cells or these t-cells and the overall response is to produce antibodies in response to that right or to produce memory b-cells and we can also produce memory t-cells I didn't talk about those enough but again these are effector T cells but you also can make as a response to this whenever they proliferate you also can make memory th2 cells and those memory th two cells will have a TCR specific to that foreign
antigen alright whenever the MHC molecule comes back MHC two molecule in the foreign antigen on the macrophage comes to him again he'll be ready for it alright that's humoral immunity what is cell mediated immunity cell mediated immunity is due to the it's going to be exerted by this cytotoxic T cells and the cytotoxic T cells they're gonna act on cells that have already been virally infected so they've been infected by a virus and there's no turning back or they're cancerous what's the overall result again one is it can actually down regulate the class 1 molecules
or it can produce the expression of a viral peptide that combined with our own self peptide and then what happens our t cytotoxic T cells recognize those either foreign peptides or they recognize the lack of class war molecules as there's not that many and then what will they do they'll produce perfer ins which would create holes in the membrane and granzymes which initiates this a pathetic mechanism that we talked about right so that's killing the cell why is it cell mediated though because the actual infectious pathogen is already inside of the cell it's not outside
of the cell it's inside of the cell and it's affected it inside of the cell okay that's the basis way or the basic way of understanding cell mediated immunity we also talked about natural killer cells but remember just because I included them with the adaptive immune system that doesn't mean they are a part of them they are not a part of the adaptive immune system they're a part of our innate immune system they're not specific but they're mechanism is very similar to the cytotoxic T cells how they do this what do they do there's three
rep mechanisms one is they either recognize that there is no MHC one molecules present and if there's no class 1 molecules present they perceive it as form because all nucleated cells have class 1 molecules and then what it'll produce perforin and granzymes and kill the cell it'll also recognize an abnormal form of the MHC molecule right and again we said MHC molecules have alpha 1 alpha 2 alpha 3 chains as well as a beta 2 microglobulin mica has no beta 2 microglobulin so therefore he's kind of like an image see if he's recognized but the
natural killer cells he'll actually really spur friends and granzymes and kill him and then again if there's any type of foreign antigen with IgG antibodies bound the natural killer cells release parens and granzymes and kill him again guys this pretty much gives us everything we're going to need to know about the entire overview of what the adaptive and the innate immune system all right ninja nerds
