all right Ninja nerds so in this video what we're going to do is we're going to talk about adaptive immunity so we've already talked a lot about the inflammatory response right we discussed it in very very very great detail now what we're going to go ahead and do is we're going to take a look specifically inside of the lymph node if you remember do you remember we had those macro phases and those neutrophils and what we're happening let's look remember if we come over here we had the macras right here and remember what these macrofagos were doing they were carrying with them what the antigen right but they were carrying it on its actual membrane surface how remember what they had on their membrane surface right here they had MH C2 molecules right so mhc2 molecules and with that they had the foreign antigen that they actually pulled away from that bacterial microb right and then what else the fils actually exocytosed their antigens into the extracellular fluid so now what we're going to do is we're going to follow these free antigens and then we're going to follow this antigen presenting cell into the lymph node and let's get in it all right so here we go so these guys are going to come in here now they're going to flow in here and let's go ahead and take a look over here so what kind of cells if we're looking inside of the lymph node the lymph node has these things called germinal centers right and germinal centers are where there's a large amount of B cells this cell right here is called a b lympo site now the B lymphocyte has specific types of receptors that are present on its cell membrane right what are these receptors right here called they're actually called B cell receptors or uh B cell receptors are usually designed to be what's called um antibodies specific type of antibody is igd antibody and we'll talk about those in a separate video but again what are these things right here called they're called B cell re ctors and what happens with these B cell receptors is these B cell receptors are formed in a very special way they undergo recombination and when they undergo this recombination you know the DNA with inside of the B cell it can actually undergo shuffling it can do the same thing that those mhc2 molecules mc1s do where it can Shuffle its DNA and produce different types every single one of these B cell receptors are different in their binding domain so they can bind different types of antigens again what do I mean by that let's say I have three different types of antigens a circle a square antigen and a triangular antigen and these are from the bacteria and they're just circulating in here right we'd have to have a B cell receptor that would fit perfectly for the circular antigen we'd have to have a square shaped receptor to fit this Square antigen and we'd have to have a triangular shaped B cell receptor to fit the Triangular antigen that's what all of these guys are they can undergo specific recombination to form different B cell receptors so now what was that thing circulating in here here was our antigen our free antigen right so we had these free antigens that were circulating in this area and by random chance that free antigen will bind onto a B cell or a B lymphocyte with the B cell receptor perfectly designed to fit that antigen by random chance and when it binds on to this it can signal different types of uh signaling mechanisms into this actual B cell's nucleus activating the B cell because you know previously this bosy is technically naive it's a naive bosy meaning it has receptors but it hasn't undergone a specific activation mechanism yet so it hasn't undergone it its immunogenicity response yet so now it's going to become active and it's going to become a little bit more mature so now what happens to this bosy this bosy will do what's called receptor mediated endocytosis what does that mean that means it'll actually take in so imagine again remember that thing the pseudopods so what will happen here let's say the antigen actually or that uh red antigen binds over here too so it comes over here and binds to this surface right here then what happens the cell membrane does those things where it makes those pseudopods right so it makes those pseudopods or it actually does another mechanism where it pulls the membrane down by binding these things called Clin and we form these Cline coated pits and then we form these Cline coated vesicles right and it pulls it inside now so now we have this endosome inside here and what's inside this we have the B cell receptor with the foreign antigen bound to it and then what can happen is on chromosome number six of the B cell what can he do he can produce a specific molecule that specific molecule fits perfectly to that antigen and look what it is we already know what this one is we already talked about him he's an mhc2 molecule and then he can come up and get fused onto the cell membrane so again what will happen with this B cell right here look it'll actually become activated and whenever it's activated what does it have on its cell membrane it has these B cell receptors right but we want that one b cell receptor that we responded to we want us to be able to make more specific types of antibodies specific to that right there so again what do we expose up on the cell membrane we expose up on the cell membrane a MHC 2 molecule again what are these things called B cell receptors and again usually they are I G D antibodies and with this mhc2 molecule what do we have exposed with it we have that foreign antigen so again this is our bosy so our bosy has become activated but it can't undergo proliferation yet it's been activated so now it is activated so we have an activated bosy how did that bmy get activated the free antigens bound on the B cell receptors are the igd antibodies trigger triggered an intercellular mechanism to activate this B cell right then what happens is the B cell will actually undergo a cline coded mediated process called receptor mediated endocytosis where it pulls the antigen and the antibody complex inside and then on chromosome number six it'll make mhc2 molecules to bind with that foreign antigen and presented on top of the cell surface so now what is this guy he is an antigen presenting cell what are the three types of antigen presenting cells again he's an antigen presenting cell so B lymphocytes macrofagos and dendritic cells so now he wants to start proliferating but we can't do that yet why can't we do that yet this is where we need to talk about our macras now so this step can't occur yet until we have some type of stimulus let's talk about that what stimulus is all right so again this maccrage let's track him look at him he's coming over here and now what is he going to do so again what was on that maccrage that maccrage if you remember so here's the maccrage there's its genes right there's it DNA with the specific genes and then what did it have Exposed on its cell membrane it had the MHC two molecules so MHC two molecules with a specific foreign anen right and again just to continue with everything that we talked about before what would it also have on its cell membrane surface it would also have a MH c one molecule with some type of specifically self antigen right so all nucleated cells will have mhc1 and these antigen presenting cells will have mhc2 molecules now this guy what does he do he comes and he presents this mhc2 molecule and the foreign antigen to a specific type of t- cell so let's draw that guy right over here so look at this guy here's our t- cell now technically this is a naive t- cell all right let's actually let's go over this so This is actually a naive T helper cell so again what does that mean by it's naive it means it has receptors that can respond to these molecules but it's not activated yet it's not specific it doesn't know exactly what it's actually going to go into and differentiate into so now what happens this mhc2 molecule there's a specific molecule that has to recognize this hc2 let's make this T Cell a little bit longer so again what is that molecule called that interacts right here look at this guy he is a let's make him a green molecule so look here here's this green molecule and it fits perfectly with this mhc2 molecule then it has a blue molecule a blue molecule that fits perfectly to that foreign antigen what are the these two proteins called this blue protein that fits perfectly to the actual foreign antigen is called a T Cell receptor sometimes they just denote it TCR so it's TCR positive right this is a TCR positive cell what is this green protein right here called this green protein right here is actually called cluster differentiation protein four so this is called a CD4 so this is a CD4 positive all right CD4 positive cell so now look at this we have a naive T helper cell the t- cell receptor reacted what is this red molecule again let's actually denote what that red molecule is that red molecule is the foreign antigen so it's the foreign antigen the foreign antigen is interacting with the T Cell receptor specific to that antigen what do I mean a again every single t- cell will have different types of t- cell receptors specific to each type of antigen let's make this more clear we have a circular antigen Square antigen triangular antigen each type of TCR is specific to this type of antigen so if it's actually so that's a blue protein right if this is the TC if that's the antigen the TCR has to be this shape if the the actual antigen is square shape the T TCR has to be specifically this shaped and if the antigen is this shaped then the TCR has to specifically be this shaped and what is that due to that's due to recombination switching and shuffling those genes due to what's called rag one and rag two genes which are recombination enzymes we'll talk about that in t- cell development which are producing these different types of t- cell receptors okay so this guy just happens to run into the perfect t- cell that can fit that antigen now what happens there's one more thing that needs to happen there is proteins inside here they're called CD3 molecules it's called CD3 and the CD3 molecule is actually going to kind of act as a uh a signaling molecule inside the cell we'll talk about him in just a second but there's another molecule that we have to talk about over here it's going to have this big big big molecule here that's actually going to be present on the T Cell let's actually make him smaller then let's actually make him like this so here's the T Cell it has a specific molecule present on its cell membrane and this molecule is called cd28 cd28 and then on the maccrage it has a specific protein that can stretch and interact with that so look at this look at that protein right there this protein right here that interacts with cd28 is called B7 so again what two proteins interacted here we have B7 interacting and we have cd28 interacting when they interact this triggers a co- stimulation reaction so again this this reaction right here this is the primary stimulation mhc2 with the CD4 t- cell receptor with the foreign antigen activates CD3 that's going to send signals to the nucleus so here is our actual nucleus with the specific specific DNA with the genes specific to each type of cyto we're going to produce that's the primary signal so this is our primary signal the co- stimulatory signal or the secondary signal is going to come from the interaction between B7 on the maccrage and cd28 on that naive T helper cell so this is called what is this again called This is called Co stimulation once we have this primary signal in this co- stimulation there's one more thing and then we're getting into the good stuff this guy starts secreting a specific protein it secretes a specific protein this maccrage and this secretes a molecule which is called inter Lucan one and interlukin one comes and binds onto a specific receptor on the actual T helper cell so interlan one binds onto this receptor and it also sends another signal so that's our third signal so we have a third signal here holy crap that's a lot of signals right so we have a primary signal here due to the mhc2 and the CD4 interaction we have uh the antigen for an antigen in the t- cell receptor activating CD3 we have the B7 with the cd28 activating co- stimulation and then we have interlukin one secreted by the macras which triggers another third signal now what happens now that te- cell has become activated so when he becomes activated he starts actually so now this t t helper cell is no longer naive he's an activated te- cell and he starts secreting it activates certain genes all these signals activates certain genes and these genes lead to the production of interlan 2 and interlukin 2 can actually come back over here and bind on its own self so what is this called whenever something works on the same cell that secreted him it's called an autocrine so this inter Lucan is an autocrine it works and activates this which sends another signal back here activates these genes and these genes start producing Another cyto Kind this cyto is called inter Lucan 4 and then there's another cyto kind is produced also with that which is called inter Lucan five now what's very very important here that we really really understand is is that whenever these interactions are occurring a naive t- cell a naive t- helper cell can actually turn into two different types so that's why I wanted to mention it let's say I have t- Helper and I put like that for the naive right he can either turn into two different types of cells a t- helper one or a t- helper two cell right in order for this to happen the t- helper not is going to have to get stimulation if it wants to become a t- helper too it has to get stimulation from what's called interlan 4 so interlukin 4 will also have to stimulate this process to occur if it wants to turn into a t- helper one cell it needs to get simulation from interlan 12 and then it can drive this process okay so again we want to make t- helper to that's who we want to make so we need interlukin four stimulation so this naive T Cell actually turned into a t- helper 2 cell so it's genes that are going to be activated the ones that we listed interlan 2 interlukin 4 interlukin 5 if we were to activate t- helper one we would activate the gamma interfere on genes and we would activate the genes to produce tumor necrotic Factor Alpha so that's why we definitely want to focus on the T helper cell and the reason why is these two factors we absolutely need those and now explain why in just a second so again let's erase this so again remember that so now we've produced interlan 4 and we've produced interlukin 5 now what happens here with these molecules well first off even before that you see how interlukin 2 comes and stimulates this this cell right here and there also be stimulation from another one that we just mentioned with which could be interlukin 4 before it even starts releasing interlan 4 and interlukin 5 it starts dividing right so this t- cell will undergo a lot of Divisions and what was that stimulus it was interlukin 2 and interlukin 4 those were the stimuli in order for this naive t- cell to become activated and turn into T helper 2 cells and then what happens these T helper 2 cells they start secreting interlan 4 and they also start secreting interlan 5 so more specifically like let's erase this here because there is interlukin 4 and5 being secreted but it's not really being secreted from a naive te- cell it's being secreted by by these mature t- helper cells so again what will these guys be secreting they'll be secreting interlan 4 and five so interlan four and interlan five so again I wanted to make sure that I very very I clarify that up very very specifically because technically interlan four and five are actually produced by the activated or proliferated form of the t- cells the t- helper two cells because this was a naive t- helper cell so it responds with all of these primary co-stimulatory and third signal releases interlukin 2 gets stimulation from interlan 4 and that interlan 4 will act what interlukin 4 interlukin 2 will act on this actual naive t- helper cell and turn on the genes to produce interlan 4 and interlan 5 to to make t helper 2 cells if it wanted to make t- helper 1 it would have secreted interlukin 12 but we didn't we made interlukin 4 now what happens with this interlukin four and five remember this B activated bosy that we couldn't have proliferate yet now we can proliferate him so what happens here here's our activated bosy the first signal is interlan 4 inter Lucan 4 comes over and activates this B turning on genes to start proliferating so now what happens we start making tons of B cells here so we're going to have a ton of activated B cells so look we have activated B cells here they're no longer naive and what's special about these B cells these B cells we've proliferated them to have bcrs specific those igd antibodies those bcrs are specific to that for an antigen super specific here okay so now it's going to have bcrs here specific to that antigen and what else will it also have it'll also have those mhc2 molecules right here with the forign antigen Exposed on the surface right so now again what would have mhc2 molecules with the foreign antigen and it will also have the B cell receptor specific to that foreign antigen then what happens interlan 5 stimulates all of these what is this called right here I actually should explain this first what is this called whenever these B cells start dividing this right here when interlukin 4 stimulates this step right here right this is called clonal expansion so this right here is called clonal expansion so these guys are going to expand and undergo ex excessive proliferation making tons of these B cells activated and now these actual B cells are immunocompetent and specifically able to recognize any type of foreign antigen because of these specific B cell receptors now interlan 5 activates these B cells and causes them some of them to start differentiating so what happens interlan 5 actually works right here right interlukin 5 actually works specifically at that step right there and then what happens now some of these B cells start undergoing differentiation and they turn into a specific type of B cell so again what is this guy right here called he's got a very very prominent very very prominent um rough endoplasmic reticulum that with these lines here these are called plasma cells now it can actually um whenever it differentiates it can differentiate also into memory B cells so there's two different types of cells that can actually be formed from this process whenever interlan 5 causes differentiation he works on these expanded clonally expanded B cells and causes some of them to turn into memory B cells with that specific B cell receptor ctor common to that foreign antigen so that we are ever exposed to it again it is ready for that so now it has a specific B cell receptor that will always be ready to respond to that that antigen ever again a second exposure third exposure Infinity exposures right the other ones will become affector cells or plasma cells and these plasma cells there is actually one more interlan that can be secreted here called interlan 6 and interlan 5 and interlan six can actually stimulate these plasma cells stimulate the plasma cell formation and interlan 5 and interlan 6 can also stimulate the plasma cells to start secreting antibodies so it starts secreting antibodies and what are these molecules right here these are antibodies and it can cause these these antibodies that are being secreted guess what these antibodies that are being secreted are going to be specific to that foreign antigen very very specific to that foreign antigen what do I mean let's go back to this again let's say here's the antigen it's a circular antigen Square antigen star antigen what happens these antibodies are specific and I'll explain why in the future videos that they have a specific variable region that can actually change from antibody to antibody in other words again recombination you can Shuff Shuffle the DNA to produce different types of antibodies with different types of variable regions which combine to different types of antigens so these antibodies being produced here by these plasma cells they are specific to that foreign antigen from that microb that we've been dealing with this whole time it's so beautiful how all this stuff is interconnected right so now what can these antibodies do these antibodies can bind on to these antigens some of these antigens might be bound to specifically a back bacteria that bacteria that we were dealing with before or it could be free antigens all right and then what can happen with that tons of things can happen with that and we'll get into more detail in that when we talk about antibodies and what they can do just in general I'll write this list down but I'll explain it in more detail in the antibody videos it can actually bind to this it can bind to all let's say here here's all the antigens on that bacteria these antibodies could bind to every single surface here and if they bind to every single surface they block this bacteria from maybe attaching to certain types of our healthy host cells and damaging it right that's called neutralization so it can neutralize this bacterial or viral molecule right let's say that this antibody binds with this freely circulating antigen and it actually causes a precipitation out of the actual reaction so we have what's called a precipitation reaction so a precipitation reaction could could actually enhance opsonization but it also can cause problems because sometimes if there is free antigen antibody complexes there is a chance that they can get deposited into tissues and cause a type three hypers sensitivity right so precipitation neutralization what if those antibodies bind on to that same bacteria remember that bacteria that we talked about in the complement system now this might be coming back a little bit right what was that complement system able to do you were able to produce a a whole bunch of different proteins and what were those proteins able to do they were able to produce a membrane attack complex and that membrane attack complex caused Lis of the cell so that's another thing that could happen there could be Lis there could be precipitation there could be neutralization one other thing let's say that you get mismatched blood remember whenever I talked about that in blood we talked about mismatched blood transfusions if you have red blood cells that you aren't supposed to have you can actually have so let's say here's the antigens let's say that this person gave they were given incompatible blood you can have antibodies that could literally bind these actual points right here and cause the actual red blood cells remember when there's an antigen antibody complex what is that called it's called a glutin a glutin so again what do we have so far we have a glutation we have neutralization we have precipitation we have Lis one more I'll talk about but again we'll get into this in more detail when we talk about this in antibodies what if I have this right here that antigen binds there and then when that antigen bind when the antibody binds to the antigen it can activate maybe do two things let's say we have two factors that it could affect here so it binds there one activates complement system remember the whole complement system and it could stop at c3b and if it stops at c3b it can activate our actual macres to come in start eating that because it has c3b receptors that's one thing what is that called and again it could also just do directly with the actual macrofagos so the macras could actually just eat this directly and what is this process right here called This is called opsonization all right so so far we have a ton of things that's happened here these antibotics can cause neutralization reaction they can cause a precipitation reaction they can initiate Lis of the bacteria or certain types of fungi they can cause an utenation reaction and some type of mismatch blood transfusion or we can even opsonize them in making it tasty right so again if this was that foreign bacteria that we talked about let's say that that was that foreign bacteria what can happen we can do an antibody mediated opsonization just right here or we can do complement up to c3b and then that enhances the opsonization also right so that's going to go back to how our adaptive immunity links up with the anate immunity now real quickly you see all this right here that we talked about with those free antigens those free antigens and how that whole pathway of how we actually took them in expressed them on class two went throughout this whole proliferation process and how we also depended upon these T helper cells to produce all these cyto kindes this right here that we have talked about is called humoral immunity that's what this is this is humoral immunity humoral immunity is in a nutshell basically everything we talked to up to this point with the B cells being activated by the free antigens then responding to these actual cyto kindes from the maccrage interacting with the T helper cell becoming activated in t- helper 2 producing inter Lucin 4 interlan 5 interlan 6 and causing these B cells to proliferate and produce antibodies that is all the humoral immunity response now we got to talk about one more type of immunity for the Adaptive and that is our cell medium Med immunity which is mediated through cytotoxic tea cells so now let's say here let's say that maccrage let's say I had a maccrage um or a t- helper cell that happened to get um infected by cancer let's say that there was actually a cell here let's just say here in general not even that just say there's a general cell here here's our general cell and this cell has been infected with cancer let's say it's a cancerous infected let say it could be cancerous could be viral so if there's a cancerous cell or a viral infected cell again what do all nucleated cells have they have class one molecules M H C class one molecules and then what else do they have exposed with it they have a self antigen there's another type of T cell that we haven't talked about yet look at this guy this is called a t cytotoxic cyto toxic cell so these are t-cytotoxic cells so these t-cytotoxic cells are very very picky they love to recognize class one molecules so they have a specific protein here that's designed to recognize these class one molecules right and they have another protein which is called a TCR but this TCR normally you don't want it to recognize your own self antigens because and we'll talk about why and t- cell development because it could lead to autoimmune diseases or just damage to your own tissue cells so now what happens in cancerous infected cells or viral cells two things can happen let's say that this is a virus infected cell if it's a virus infected cell so if this was infected with a virus viruses can actually sometimes get integrated into our own DNA and can lead to the production of viral proteins and those viral proteins are endogenous proteins and these endogenous proteins can actually get integrated onto this self- peptide so look what can happen here I can actually have a self peptide and this viral peptide added on there if that happens and this t-cytotoxic cell has it what is this red protein called this red protein is called cd8 positive protein right and what is this actual black protein right here called this black protein is called a TC or T Cell receptor if this and there's a self peptide here which is the blue one and then this viral peptide which is added right there now let's say by chance this TCR recognizes that Viral peptide there so recognize there's something funky with this cell this cell's cancerous or it's virus infected right then what's it going to happen it's pissed it's going to do something about this right so now it's going to activate this guy and he's going to start producing specific types of proteins what are these proteins called one of them is called perin now perin are basically going to prod produce holes inside the membrane so imagine I draw here A whole bunch of little black proteins here creating holes inside of the cell membrane then what happens it produces another molecule and this molecule is called granzymes so now granzymes will actually move through these pores and when they move through the pores they'll come in here and they'll activate a specific set of genes what are those genes called they're called pro-apoptotic genes so they're called pro-apoptotic genes so there's a set of genes in here that are going to be activated now I'm going to show the exact mechanism of the apoptosis here quick so again here's the DNA and again what's happening there's going to be granzymes floating in here activating a set of genes which are called the proapoptotic genes these pro-apoptotic genes what is apoptosis actually apoptosis is programed cell death right so how is it going to do it it's going to activate this set of genes here these proapoptotic genes and these genes are responsible for producing a protein called back and what happens what else do we have inside here we also love to have mitochondria right so we have a mitochondria in here now what's so special about the mitochondria on the mitochondria there's a specific protein here this Protein that's actually inside of the cell I'm sorry with inside of the actual membrane this is a phospholipid B layer though of the mitochondria that protein is called a bcl2 so it's called b 2 what happens is back is actually a protein imagine them like this so imagine backx is like this so again what is this thing right here called backs backs will actually bind onto the bcl2 and pull the bcl2 out so then when bcl2 is pulled out so let's imagine I I do that over here let's say I have backs over here he Yanks out the bcl2 so he pulls out the bcl2 at pulls it right out and then look what happens here there's a molecule in here called cytochrome C and when cytochrome C gets out here it activates cast bases and then these cast bases can start causing proteolytic destruction of multiple things with inside of the cell and eventually cause the cell to die and what is that called This is called a hosis so again this is called cell mediated immunity and how is that regulated it's regulated through the cytotoxic tea cells right either by recognizing these uh foreign endogenous viral antigens or maybe even cancerous antigens bound with the self peptides this would be for cancerous cells viral cells and one more thing cell mediated immunity just think about it like this it's occurring because these things these viral or pathogenic molecules are inside of the cell they're damaging the cell they've already caused a lot of damage inside of the cell it's an internal problem humoral immunity is an external problem what do I mean by that it was a free antigen that actually activated this B cell to start undergoing this whole proliferative process so humoral immunity kind of think about the humoral fluid so it's occurring because of free antigens causing this process whereas the antigens in this case are endogenous and are occurring inside of the cell where the actual humal is exogenous okay now let's finish up with the natural killer cells but remember natural killer cells are not a part of our adaptive immunity and I'll explain why so natural killer cells are just basically large a granular lymphocytes now they can kill by three ways let's say here I have a cell another cell and another cell each one of these cells have three different types of reasons why it would be killed one is kind of going off of what this guy had let's say that this guy has no [Music] mhc1 molecules expressed on the surface because you know all nucleated cells should have mhc1 molecules you have to know that next thing what would be this next molecule this next molecule right here is called Ma and and Ma is just a different type of mhc1 molecule it's similar to it real quick MHC molecules usually have a specific type of structure here they have what's called an alpha 1 an alpha 2 an alpha 3 and a beta 2 structure that's the structure of MHC molecules they usually have an alpha 1 Alpha 2 Alpha 3 and a beta 2 molecule in MA there's no beta 2 okay so it's kind of like mhc1 or mhc2 but it's lacking the beta 2 microG globin so what happens here if they recognize the ma they're going to kill it that way okay what's the last one it could also do it through IGG mechanism so remember that there's some type of foreign antigen here and then there is a i g g antibody then it can also recognize this cell and kill it how does it kill it the same way the cytotoxic tea cells do what will it do it will release perence what will these perin do create holes inside of these membranes and then it'll secrete granzymes and the granzymes will do what the granzymes will act on the proapoptotic genes activate backs backs will then pull bcl2 out of the mitochondria opening it up for cytochrome C to come out and then cytochrome C will then cause activation of cast bases and lead a proteolytic destruction of the cell right and cause apoptosis so again one more time guys let's finish up here and let's recap everything just a a general overview of this humoral immunity and cell mediated immunity are part of your adaptive immunity right humoral immunity again how would you explain that it's due to freely circulating antigens things that are outside of the cell exogenous exogenous means it's actually an antigen that's actually outside of the cell right it is an exogenous protein so the problem here is with things outside in the fluid remember who released all those free antigens into the fluid it was the neutrophils and whenever that happened it activated the B cell from the external side and then triggered all this Cascade events right in order for this B cell to get activated but what else had to happen here we also had to have the maccrage come over here present his mhc2 molecule in the foreign antigen and it's still external it's not inside of the te- cell it's going to Signal these act it's going to produce signals to activate the t- helper cell to produce a ton of different types of inter lucans and cyto and those will be interlan four interlan 5 and interlan six and what are they trying to do they're trying to activate the B cells to switch on the genes to produce antibodies that whole event is humal immunity and it's all designed to take care of the things that are outside of the cell in the humoral fluid we call it right cell mediated is a problem with things inside of the cell endogenous molecules like due to viral proteins or cancerous peptides that are produced as a result right those are going to be the problem because it's inside of the cell it's already invaded infected and actually caus damage to the inside of the cell there's no going back for this cell it's done it's destined for death so cytotoxic tea cells have to deal with that right by eliminating these cells because the problem is inside of the cell and there's no turning back that's cell mediated immunity and that is a that's only done by cytotoxic T cells remember the natural killer cells are not a part of your adaptive immunity I just wanted to show you that their mechanism is very similar to cytotoxic tea cells and show you how they recognize it differently but remember natural killer cells are part of your innate immune system because they can actually react with no class one or MAA which is lacking a beta 2 microG globin or IGG antibodies so again in a nutshell that pretty much covers everything on adaptive immunity now if you click on the Right video here in the corner we're going to do an entire overview all right of inflammation part one inflammation part two part three part four and adaptive immunity and if I keep it under 20 minutes guys I get a prize all right Ninja nerds