ATAR Notes: Forum
VCE Stuff => VCE Science => VCE Mathematics/Science/Technology => VCE Subjects + Help => VCE Biology => Topic started by: duhherro on June 03, 2012, 07:34:03 pm
-
Hi guys , having a bit of trouble with T-helper cells, do they just immediately identify foreign pathogens or come into action when a macrophage puts up the MHC marker to stimulate T helpers ?
Thanks in advance!
-
generally it will be an APC (antigen presenting cell) that will stimulate the t helper cell and cause the cascade of events that follow
-
generally it will be an APC (antigen presenting cell) that will stimulate the t helper cell and cause the cascade of events that follow
Thanks for the fast reply!
Are APC's just macrophages ? or jut any phagocyte?
-
dendritic cells are probably the most common (for VCE purposes anyway) i think the only function of the dendritic cell is to present antigens
then the macrophages is the next most common.
both do the same tho in terms of presenting the antigen
-
dendritic cells are probably the most common (for VCE purposes anyway) i think the only function of the dendritic cell is to present antigens
then the macrophages is the next most common.
both do the same tho in terms of presenting the antigen
So dendritic cells are a type of lymphocyte? Just engulfs a foreign particle, then display its own antigen? And how do they display their antigen and marker 1 or marker 2 etc?
-
DCs are technically a type of lymphocyte, but they're not typically discussed as such. When someone says lymphocyte, they usually refer to T/B cells.
DCs are excellent at phagocytosing material from the environment. It then gets degraded within the cell and the peptide fragments merge with empty MHCII molecules. The complex is then displayed on the cell surface. They can do the same thing with MHCI, just via a slightly different presentation pathway.
-
DCs are technically a type of lymphocyte, but they're not typically discussed as such. When someone says lymphocyte, they usually refer to T/B cells.
DCs are excellent at phagocytosing material from the environment. It then gets degraded within the cell and the peptide fragments merge with empty MHCII molecules. The complex is then displayed on the cell surface. They can do the same thing with MHCI, just via a slightly different presentation pathway.
I see, cleared a lot! So then a T-helper comes and binds to it , which stimulates the profileration of B cells into plasma and B-memories? And at the same time, T cells will be stimulated, forming Cytotoxic and T-memories ? Could you just verify that for me haha ^^
-
yes, in an exam they seem to ask about the t helper cell integrating with bcells with clonal selection/expansion than integrating with tcells.
-
edit
^^
ligands beat me but here anyway
I see, cleared a lot! So then a T-helper comes and binds to it , which stimulates the profileration of B cells into plasma and B-memories? And at the same time, T cells will be stimulated, forming Cytotoxic and T-memories ? Could you just verify that for me haha ^^
Th cell binds and is activated. The Th cell then goes off to find a B cell and activates it. The B cell will either produce antibodies or become a memory cell. And yes, at the same time, CD8/Tc cells will be generated :)
-
edit
^^
ligands beat me but here anyway
I see, cleared a lot! So then a T-helper comes and binds to it , which stimulates the profileration of B cells into plasma and B-memories? And at the same time, T cells will be stimulated, forming Cytotoxic and T-memories ? Could you just verify that for me haha ^^
Th cell binds and is activated. The Th cell then goes off to find a B cell and activates it. The B cell will either produce antibodies or become a memory cell. And yes, at the same time, CD8/Tc cells will be generated :)
Thanks!!! Whew I'm glad i'm right for once LOL. and HOLY hell, so now a TH cell binds to the engulfed particle but then leaves and activates B / T cell stimulation into cloning? !!!??
-
edit
^^
ligands beat me but here anyway
I see, cleared a lot! So then a T-helper comes and binds to it , which stimulates the profileration of B cells into plasma and B-memories? And at the same time, T cells will be stimulated, forming Cytotoxic and T-memories ? Could you just verify that for me haha ^^
Th cell binds and is activated. The Th cell then goes off to find a B cell and activates it. The B cell will either produce antibodies or become a memory cell. And yes, at the same time, CD8/Tc cells will be generated :)
Thanks!!! Whew I'm glad i'm right for once LOL. and HOLY hell, so now a TH cell binds to the engulfed particle but then leaves and activates B / T cell stimulation into cloning? !!!??
the TH cell binds to the antigen on the APC, it then releases cytokines (an interleukin of some sort i think, don't need to know that) that attract tc/bcells (the TH cell hasn't left the APC yet) and it then looks for the complementary fit for the antigen
in most of the practice exams so far its been mostly TH cell binding to an APC then attracting a bcell and you have to show it proliferates/differentiates ect more so than tc cells
(http://www.biology.arizona.edu/immunology/tutorials/immunology/graphics/clon_selection98.gif)
-
edit
^^
ligands beat me but here anyway
I see, cleared a lot! So then a T-helper comes and binds to it , which stimulates the profileration of B cells into plasma and B-memories? And at the same time, T cells will be stimulated, forming Cytotoxic and T-memories ? Could you just verify that for me haha ^^
Th cell binds and is activated. The Th cell then goes off to find a B cell and activates it. The B cell will either produce antibodies or become a memory cell. And yes, at the same time, CD8/Tc cells will be generated :)
Thanks!!! Whew I'm glad i'm right for once LOL. and HOLY hell, so now a TH cell binds to the engulfed particle but then leaves and activates B / T cell stimulation into cloning? !!!??
the TH cell binds to the antigen on the APC, it then releases cytokines (an interleukin of some sort i think, don't need to know that) that attract tc/bcells (the TH cell hasn't left the APC yet) and it then looks for the complementary fit for the antigen
in most of the practice exams so far its been mostly TH cell binding to an APC then attracting a bcell and you have to show it proliferates/differentiates ect more so than tc cells
(http://www.biology.arizona.edu/immunology/tutorials/immunology/graphics/clon_selection98.gif)
Hmm Ligands, I understood the part where you got up to the 'releasing cytokines that attract t/b cells ' so then the TH unbinds from the antigen on APC and starts to look for a complementary fit for the antigen? Just a bit unsure on what you mean by looking for a complementary fit for the antigen.
Excuse my thick head :S
-
for example if you have a flu vaccine with the flu antigen the dendritic cell/macrophage is going to engulf this and display it on there MHC 2 marker. the TH cell will then bind to this MHC 2 marker, if in this case its going to be a bcell, there going to find an antibody on the bcell specific to the antigen (complementary in shape to be able to bind), cannot have the same shape - will not bind obviously, similar to competitive inhibition in enzymes
im not the best at explaining things
-
for example if you have a flu vaccine with the flu antigen the dendritic cell/macrophage is going to engulf this and display it on there MHC 2 marker. the TH cell will then bind to this MHC 2 marker, if in this case its going to be a bcell, there going to find an antibody on the bcell specific to the antigen (complementary in shape to be able to bind), cannot have the same shape - will not bind obviously, similar to competitive inhibition in enzymes
im not the best at explaining things
Don't worry, i understood that :D.
So the production of antibodies will also bind to the APC with the TH cell ? And antibodies simply just "limit the movement" of the APC so more phagocytes and destroy it easier?
Also , when you said about the "in this case MHC 2 - b cell" , does that mean if the TH cell that binds to an APC with MHC 1 will result in stimulation of the T- cell side of immunity (cytotoxic + memory) ?
-
MHCI = CD8 activation (cytotoxic)
MHCII = CD4 activation (helper)
If you can't remember you can use the rule of 8, where if you multiply the MHC number by the T cell number it has to equal 8 (1*8 and 2*4)
As for what happens in binding.
Flu vaccine is given. It has dead flu virus in it. The virus is taken up by an APC and broken down. It's displayed on the cell surface on MHCI and MHCII. T helper cells arrive and bind MHCII, being activated. They then bind to a B cell and activate the B cell. The T cell will dissociated from the B cell and continue activating other B cells. The activated B cell will produce antibodies or form a memory cell. Produced antibodies will go into the circulation and have a protective effect for when you do get infected with flu.
-
MHCI = CD8 activation (cytotoxic)
MHCII = CD4 activation (helper)
If you can't remember you can use the rule of 8, where if you multiply the MHC number by the T cell number it has to equal 8 (1*8 and 2*4)
As for what happens in binding.
Flu vaccine is given. It has dead flu virus in it. The virus is taken up by an APC and broken down. It's displayed on the cell surface on MHCI and MHCII. T helper cells arrive and bind MHCII, being activated. They then bind to a B cell and activate the B cell. The T cell will dissociated from the B cell and continue activating other B cells. The activated B cell will produce antibodies or form a memory cell. Produced antibodies will go into the circulation and have a protective effect for when you do get infected with flu.
Ohhh, could you just expand a bit on the ..
MHCI = CD8 activation (cytotoxic)
MHCII = CD4 activation (helper) parts
So if an APC displays a MHC 1 marker, does that mean cytotoxic T cells just come and bind to it and then puncture the APC's membrane and hence no antibodies are formed?
And when you mentioned about the T cell dissociating from a B-cell , does that mean just the B cell becomes unbound and then forms plasma cell/memories and then the APC with the attached TH cell just binds to another B-cell and the process repeats til antibody levels are high enough to destroy all foreign stuff?
-
APCs display MHCI and MHCII. It's just that cytotoxic cells only bind MHCI and helper cells only bind MHCII.
If APCs display MHCI that means that they can be targeted for destruction, yes. However, destroying the APC will not prevent antibodies being formed (unless the APC also happens to be a B cell).
Yes. Once a B cell is activated it does not need to remain bound to the T cell. The T cell, once activated, does not need to remain bound to the APC, since the APC will be needed to activate other T cells.
-
APCs display MHCI and MHCII. It's just that cytotoxic cells only bind MHCI and helper cells only bind MHCII.
If APCs display MHCI that means that they can be targeted for destruction, yes. However, destroying the APC will not prevent antibodies being formed (unless the APC also happens to be a B cell).
Yes. Once a B cell is activated it does not need to remain bound to the T cell. The T cell, once activated, does not need to remain bound to the APC, since the APC will be needed to activate other T cells.
Wow, never knew that destroying the APC will not prevent antibodies being formed, does this just mean that B cells happened to get stimulated by cytotoxic T cells too?
So when a B-cell gets stimulated by the T cell, does it just clone into millions/a lot of antibodies (1 B cell = a lot of antibodies specific to APC) ? And then the APCs will get bound by another TH cell and that process repeats again?
And speaking about antibodies, do they just simply restrict the movement of the APC so immune cells can destroy the APC more effeciently ?
-
APCs display MHCI and MHCII. It's just that cytotoxic cells only bind MHCI and helper cells only bind MHCII.
If APCs display MHCI that means that they can be targeted for destruction, yes. However, destroying the APC will not prevent antibodies being formed (unless the APC also happens to be a B cell).
Yes. Once a B cell is activated it does not need to remain bound to the T cell. The T cell, once activated, does not need to remain bound to the APC, since the APC will be needed to activate other T cells.
Wow, never knew that destroying the APC will not prevent antibodies being formed, does this just mean that B cells happened to get stimulated by cytotoxic T cells too?
So when a B-cell gets stimulated by the T cell, does it just clone into millions/a lot of antibodies (1 B cell = a lot of antibodies specific to APC) ? And then the APCs will get bound by another TH cell and that process repeats again?
And speaking about antibodies, do they just simply restrict the movement of the APC so immune cells can destroy the APC more effeciently ?
i don't think you are understanding the role of an APC, they are not part of the pathogen and are not targeted by antibodies/tc cells, they simply stimulate t helper cells
1 bcell may turn into 1billion plasma cells which may produce 1billion antibodies each with is specific to a ANTIGEN not a APC, a different APC with a different antigen will bind to a th cell in future infections for a different response.
antibodies just bind to a specific antigen - signals the non-specific immune system to increase the rate of phagocytosis
-
Thanks ligands, certainly clarified the parts i have troubled with :D. On a note , if its regarding MHC 1 and cytotoxic T cells, how would there be a production of antibodies in this scenario?
-
Thanks ligands, certainly clarified the parts i have troubled with :D. On a note , if its regarding MHC 1 and cytotoxic T cells, how would there be a production of antibodies in this scenario?
there wont be any production of antibodies if t cytotoxic cells are produced. antibodies are only b cells.
-
Thanks ligands, certainly clarified the parts i have troubled with :D. On a note , if its regarding MHC 1 and cytotoxic T cells, how would there be a production of antibodies in this scenario?
there wont be any production of antibodies if t cytotoxic cells are produced. antibodies are only b cells.
Ahh so in our body, there are Cytotoxic T cells already circulating and once a MHC 1 is displayed it will just bind to that APC and then it destroys it ?
-
Thanks ligands, certainly clarified the parts i have troubled with :D. On a note , if its regarding MHC 1 and cytotoxic T cells, how would there be a production of antibodies in this scenario?
there wont be any production of antibodies if t cytotoxic cells are produced. antibodies are only b cells.
Ahh so in our body, there are Cytotoxic T cells already circulating and once a MHC 1 is displayed it will just bind to that APC and then it destroys it ?
sort of, MHC 1 is shown by all molecules with a nucleus and is designed to distinguish self from non-self
t cytotoxic wont travel around binding to random antigens showing a non-self MHC marker unless of course it has been told to do so from the th cell.
that job is done by the non-specific immune system, eg. marcophages.
t cytotoxic are specific therefore have to be programmed, same as b cells to target 1 specific antigen otherwise they will not kill anything and are pretty much waiting to be stimulated.
-
Thanks ligands, certainly clarified the parts i have troubled with :D. On a note , if its regarding MHC 1 and cytotoxic T cells, how would there be a production of antibodies in this scenario?
there wont be any production of antibodies if t cytotoxic cells are produced. antibodies are only b cells.
Ahh so in our body, there are Cytotoxic T cells already circulating and once a MHC 1 is displayed it will just bind to that APC and then it destroys it ?
sort of, MHC 1 is shown by all molecules with a nucleus and is designed to distinguish self from non-self
t cytotoxic wont travel around binding to random antigens showing a non-self MHC marker unless of course it has been told to do so from the th cell.
that job is done by the non-specific immune system, eg. marcophages.
t cytotoxic are specific therefore have to be programmed, same as b cells to target 1 specific antigen otherwise they will not kill anything and are pretty much waiting to be stimulated.
Ahh, so that means only if the immune cells know it needs a specific response if the 2nd line of defence isnt sufficient, it will put an MHC 1 to stimulate the 3rd line (cytotoxic) to help?
Thanks again ligand + Spice!! Great help although i am annoying you guys :(
-
Ahh, so that means only if the immune cells know it needs a specific response if the 2nd line of defence isnt sufficient, it will put an MHC 1 to stimulate the 3rd line (cytotoxic) to help?
Thanks again ligand + Spice!! Great help although i am annoying you guys :(
yes and no, its generally going to go back to 3rd line because it much more efficient than the 2nd line is nearly all cases. because the 3rd line is actively looking for this specific antigen, whereas the 2nd line is more random and it may bump into whatever antigen and isn't as reliable because of that.
-
Ahh, so that means only if the immune cells know it needs a specific response if the 2nd line of defence isnt sufficient, it will put an MHC 1 to stimulate the 3rd line (cytotoxic) to help?
Thanks again ligand + Spice!! Great help although i am annoying you guys :(
yes and no, its generally going to go back to 3rd line because it much more efficient than the 2nd line is nearly all cases. because the 3rd line is actively looking for this specific antigen, whereas the 2nd line is more random and it may bump into whatever antigen and isn't as reliable because of that.
Hmm didn't quote catch that part, did you mean that when an APC engulfs the foreign particle, does it just immediately put up a MHC 1 marker?
And on a sidenote, how do memory cells even work? Do they just instantly produce antibodies when the same pathogen is encountered in the body by the same antigen on MHC marker?
-
so all cells will have a MHC 1, they don't pop up or anything
seems that the 2nd line is not stimulated to target certain antigens it may only destroy 500 (example) foreign antigens compared to the 3rd line which may kill all the same antigen in 1 hit, 5000 at a time so it is much more reliable
for memory cells we just need to know that for subsequent infection by the same antigen there will be a much faster and stronger response - these questions are generally graph type questions
-
so all cells will have a MHC 1, they don't pop up or anything
seems that the 2nd line is not stimulated to target certain antigens it may only destroy 500 (example) foreign antigens compared to the 3rd line which may kill all the same antigen in 1 hit, 5000 at a time so it is much more reliable
for memory cells we just need to know that for subsequent infection by the same antigen there will be a much faster and stronger response - these questions are generally graph type questions
I see so whenever there is a serious pathogen, it usually always stimulates the 3rd line then?
-
pretty much, or for any antigen that has not already been stimulated the antigen is presented for a response
-
The T cell, once activated, does not need to remain bound to the APC, since the APC will be needed to activate other T cells.
APC activates other T cells? What other T cells can this APC activate? The T cell that it just activated, is only specific to that APC (which has the antigen-MHC complex presented on the surface of its membrane). So why are there other T cells binding to that APC? :o
EDIT:
Oh, unless you mean the CD8+ T cells that is specific to that APC (and not OTHER T cells)? That makes sense. Otherwise, could you please elaborate further, thanks.
-
The T cell, once activated, does not need to remain bound to the APC, since the APC will be needed to activate other T cells.
APC activates other T cells? What other T cells can this APC activate? The T cell that it just activated, is only specific to that APC (which has the antigen-MHC complex presented on the surface of its membrane). So why are there other T cells binding to that APC? :o
EDIT:
Oh, unless you mean the CD8+ T cells that is specific to that APC (and not OTHER T cells)? That makes sense. Otherwise, could you please elaborate further, thanks.
Ahhh as in that one APC could bind to another TH cell to stimulate more humoral immunity. So does binding to just one APC enough to destroy all the pathogen assuming it came in large numbers?
-
I don't mean to hijack this thread, but, is there ALWAYS a lymphocyte receptor that can bind to an antigen? Is there actually an INFINITE number of B/T lymphocytes like I've heard? Your genome is limited right? So your genes can only randomize and rearrange the DNA a certain number of times? If so, hence the statement that states: "Whatever the antigen, there will be lymphocyte receptor that can bind to it!" is incorrect? It's rare, yes, maybe 0.001% chance that there will be this ONE antigen that will not have a lymphocyte be able to bind to it? Anyone care to elaborate further on this?
Thanks,
-
Well there obviously cant be an infinite number of cells. However, the question of how we generate so many is a good one. Just rearranging our genes is nowhere near enough. That's why developing lymphocytes undergo random mutations in the DNA that codes for their receptor, to increase variability aa much as possible. Furthermore, after activation, they undergo another period of mutation, in order to increase affinity and change conformation to best fit the antigen.
So whilst not infinite, the chance of seeing an antigen they cannot react with is very low
-
So whilst not infinite, the chance of seeing an antigen they cannot react with is very low
Ah. So what if there was an antigen that it could not react with. This would mean that there would be no third line of defense taking place right? What would happen then? Of course the second line would still be taking place, and phagocytes and inflammation are probably going to be the most common methods of ATTEMPTING to eliminate the infection or pathogen whilst interferons assisting in the resistance of surrounding cells and decreasing the virulence of the pathogen itself in doing so. Although, no third line will be able to take place unless and until a B-cell/T-cell is eventually developed and mutated and such, that it can finally bind to that antigen in order to create a specific response and thus a faster response to the pathogen in the mission to eliminate it?
EDIT:
Oh, and could you also respond to my previous post to clear things up:
Here
Thanks Baby Spice,
-
Ah. So what if there was an antigen that it could not react with. This would mean that there would be no third line of defense taking place right?
Hypothetically, yes. If there was an antigen that could not be bound by any lymphocyte receptors in the body, then you wouldn't get specific T cell activation etc. as they would be unable to recognize it. However, every such antigen within the pathogen would need to be unrecognizable rather than just one.
Sidenote that's not relevant to VCE but for understanding: T cells can be activated without specific MHC/peptide complex signals if a state of general inflammation exists within the body and there are sufficient inflammatory activatory signals present
Of course the second line would still be taking place, and phagocytes and inflammation are probably going to be the most common methods of ATTEMPTING to eliminate the infection or pathogen whilst interferons assisting in the resistance of surrounding cells and decreasing the virulence of the pathogen itself in doing so.
Depending on what infection it is, the innate immune system (second line) may be sufficient. Also bear in mind that interferons are generally for viral infections rather than bacterial infections
Although, no third line will be able to take place unless and until a B-cell/T-cell is eventually developed and mutated and such, that it can finally bind to that antigen in order to create a specific response and thus a faster response to the pathogen in the mission to eliminate it?
If, hypothetically, there was no T cell capable of binding and recognizing any pathogen antigens, and the innate system could not contain the pathogen, then you'd die. Your body would not attempt to develop a T cell that could response, since it's already generating a random selection of receptors for maximum coverage and protection. There's no mechanism in the body to cause developing T/B cells to develop a particular specificity.
EDIT:
Oh, and could you also respond to my previous post to clear things up:
Here
Other similarly specific cells can be activated. Bear in mind that each pathogen does not contain one, single antigen, it will contain several. So you will get activation of differently specific cells, but they'll all be specific for different parts of the pathogen. You'll also get CD4 (Th) and CD8 (Tc) activation, not just CD8 activation.
-
If, hypothetically, there was no T cell capable of binding and recognizing any pathogen antigens, and the innate system could not contain the pathogen, then you'd die. Your body would not attempt to develop a T cell that could response, since it's already generating a random selection of receptors for maximum coverage and protection. There's no mechanism in the body to cause developing T/B cells to develop a particular specificity.
Okay. Wait, so how long does an inactivated T cell exist in the body before it will die? And when it does die, the immune system / your brain does not know that right? So, upon making new T-cells, the chance of making that same T-cell with the exact same variable regions (that died), could be of any possibility/probability?
Other similarly specific cells can be activated. Bear in mind that each pathogen does not contain one, single antigen, it will contain several. So you will get activation of differently specific cells, but they'll all be specific for different parts of the pathogen. You'll also get CD4 (Th) and CD8 (Tc) activation, not just CD8 activation.
If there are several antigens present on the pathogen, that would mean there are numerous antigenic determinants on the single antigen? Hence there are quite a lot of binding receptor sites for a lymphocyte and/or APC?
--
And a few general questions, antigens, themselves, are not necessarily all foreign molecules right? Until.. they are classified as non-self or self (or is this the role of self/non-self MHC markers? Could you distinguish the difference and similarities between antigens and MHC markers, sometimes it's rather bewildering)! Thus self-antigens, thereby, don't provoke or initiate any sort of immune response at all? Or they do? And the lymphocyte that had bind to that self-antigen is then destroyed as a result of self-tolerance? But there's a very low chance of this happening right? Because before the lymphocytes are produced, they undergo a sort of "background check" don't they? To see if they will bind to self-antigens located throughout the body and if they are, they are immediately destroyed as a result?
Thanks,
-
Okay. Wait, so how long does an inactivated T cell exist in the body before it will die? And when it does die, the immune system / your brain does not know that right? So, upon making new T-cells, the chance of making that same T-cell with the exact same variable regions (that died), could be of any possibility/probability?
They have half lives measured in years, so they will be around for a long time. The organ (thymus) that produces your T cells actually degenerates in the early years of life and stops completely during adolescence, so what you make originally is generally enough to see you through. Whilst theoretically you can produce two T cells with the exact same receptor, the probability of this occurring is so negligible that it's essentially irrelevant. The population of T cells with the same receptor will have derived from clonal expansion of the original T cell, not from spontaneous production of new, identical cells.
If there are several antigens present on the pathogen, that would mean there are numerous antigenic determinants on the single antigen? Hence there are quite a lot of binding receptor sites for a lymphocyte and/or APC?
Yes. But bear in mind that T cells can never bind directly to a pathogen, they can only bind MHC and see pathogens in the context of that.
There's also terminology here, such as "immunogens" being different to "antigens" being different to "epitopes/determinants" but dw about that.
And a few general questions, antigens, themselves, are not necessarily all foreign molecules right? Until.. they are classified as non-self or self (or is this the role of self/non-self MHC markers? Could you distinguish the difference and similarities between antigens and MHC markers, sometimes it's rather bewildering)!
An antigen is anything that generates an immune response. Usually foreign molecules. Self molecules have the potential to be antigenic, but typically they don't stimulate immune responses (because of tolerance, which you ask about below).
MHC is what the cells of the body use to present antigens (or more correctly, fragments of antigens) to the immune system. T cells bind to MHC/antigen peptide complexes and that's how they see the infection etc. So MHC is the picture frame and the antigen is the picture.
Essentially it's to make it easier for the body. T cells know that whatever they need to respond to will always be shown on MHC. Therefore, they only need to be capable of binding to MHC rather than every conceivable pathogen etc.
Thus self-antigens, thereby, don't provoke or initiate any sort of immune response at all? Or they do? And the lymphocyte that had bind to that self-antigen is then destroyed as a result of self-tolerance? But there's a very low chance of this happening right? Because before the lymphocytes are produced, they undergo a sort of "background check" don't they? To see if they will bind to self-antigens located throughout the body and if they are, they are immediately destroyed as a result?
Normally they don't. When T cells are being developed there are very stringent tolerance checkpoints they have to pass (the body displays all its self antigens and if T cells respond, they get deleted). That means that only T cells that are not capable of reacting with self make it into the periphery and general circulation of the body.
That's in theory. In practice you usually get a few sneaking out now and again, so there are more mechanisms in the periphery to ensure that those that do get out and activate, cannot cause any serious damage. If those mechanisms fail as well, you get autoimmune disease (T1DM, MS etc.)
-
And a few general questions, antigens, themselves, are not necessarily all foreign molecules right? Until.. they are classified as non-self or self (or is this the role of self/non-self MHC markers? Could you distinguish the difference and similarities between antigens and MHC markers, sometimes it's rather bewildering)!
An antigen is anything that generates an immune response. Usually foreign molecules. Self molecules have the potential to be antigenic, but typically they don't stimulate immune responses (because of tolerance, which you ask about below).
MHC is what the cells of the body use to present antigens (or more correctly, fragments of antigens) to the immune system. T cells bind to MHC/antigen peptide complexes and that's how they see the infection etc. So MHC is the picture frame and the antigen is the picture.
Essentially it's to make it easier for the body. T cells know that whatever they need to respond to will always be shown on MHC. Therefore, they only need to be capable of binding to MHC rather than every conceivable pathogen etc.
Wonderful, thanks for that.
So both the classes of MHC actually break the antigen down, and present its fragments? I thought it had only been 1 of the class of the MHC that did that. Thanks for clearing that up.
And also, if it was the antigen was protein-based, usually only part of that protein or a peptide segment of it is antigenic right? Does the same go for all other types of antigens that are besides proteins?
-
Neither class of MHC breaks antigens down. In both cases the cell does it and the MHC just displays the fragments produced.
Non protein antigens are a whole lot more complex and won't really be relevant at VCE. There are other types of T cells and other types of receptors involved in things like glycolipid antigens etc. that you shouldn't worry about.
-
Neither class of MHC breaks antigens down. In both cases the cell does it and the MHC just displays the fragments produced.
Non protein antigens are a whole lot more complex and won't really be relevant at VCE. There are other types of T cells and other types of receptors involved in things like glycolipid antigens etc. that you shouldn't worry about.
I'm aware of that, bad wording on my end. Thanks.
Apologies @OP if I hijacked this thread, I hope the answers have become useful to you though.
-
Haha it is okay danny :D
Also another question, are T-helpers always produced? Or do T-cells undergo proliferation into the T-helper and Cytotoxic ones?
And what happens in a memory T-cell , do they just bind to foreign antigen on MHC 1's and just acts in the same way as a cytotoxic t-cell would ?
-
And what happens in a memory T-cell , do they just bind to foreign antigen on MHC 1's and just acts in the same way as a cytotoxic t-cell would ?
I'm confused about this sort of thing too. When T cells bind to infected cells, do they bind to the foreign antigen that the infected cell presents? And is this foreign antigen presented on MHC 1? I thought that MHC 1 are just self markers for the immune system to differentiate between self and non-self? :-\