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.)
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