Why do TCR's not undergo hypermutation

  • Thread starter FunkyDwarf
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In summary, B cells undergo somatic hypermutation to increase affinity for the antigen, and this is why T cells don't go through the same process.
  • #1
FunkyDwarf
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Hello!

I have a question regarding the development of B cells vs T cells.

Specifically, I understand that the development of the T cell receptions and antibodies on the Bcells are very similar up to the point of activation. Both undergo somatic recombination to generate diversity, but then B-cells go through an extra phase with somatic hypermutation to increase affinity.

One argument as to why T-cells don't go through this second phase as well is that it may cause them to increase their affinity for self-peptides and thus become dangerous (given that they already passed negative selection it would be like letting someone 'make' a gun once through a metal detector). Thus by ensuring the helper T-cells that don't bind to self are the ones activating B-cells, we ensure that the B-cells (having receptors for the same antigen as the t-cell) won't go out and proliferate and bind to self peptides and cause auto immune problems.

However: what's to stop somatic hypermutation in the B-cells from giving rise to antibodies that can bind to self? If the possible range of binding is so huge that it is a risk for T-cells, why is it not also a risk for B-cells? (i.e. to mutate to bind well beyond their original antigen profile)

Thanks!

EDIT: ok it makes a bit more sense on I realized that the activation comes from T cells both before and after hypermutation, meaning that a T-cell would have to present a self peptide in order to proliferate a nasty B-cell. But then the question becomes: isn't the bottleneck still the affinity of the TCRs? Or is it just a matter of 'assume the TCR can bind at some point to the antigen, let's make sure that antibodies are faster/better'?
 
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  • #2
@BillTre can probably shed some light on this issue.
 

1. Why do TCR's not undergo hypermutation?

TCR's, or T cell receptors, do not undergo hypermutation because they are already highly specialized and specific in recognizing foreign antigens. Hypermutation is a process that occurs in B cells to generate a diverse range of antibodies, but TCR's do not have the same level of diversity in their gene segments and therefore do not require hypermutation.

2. Can TCR's be artificially induced to undergo hypermutation?

No, TCR's cannot be artificially induced to undergo hypermutation. This process is regulated by specific enzymes and factors that are only present in B cells, not T cells. Additionally, artificially inducing hypermutation in TCR's could lead to harmful mutations and dysfunction in the immune response.

3. Is hypermutation necessary for T cell diversity?

No, hypermutation is not necessary for T cell diversity. TCR's already have a wide range of gene segments that can combine to generate a diverse repertoire of T cells. This, combined with the process of positive and negative selection in the thymus, ensures that T cells are able to recognize a diverse array of antigens without the need for hypermutation.

4. Do other immune cells undergo hypermutation?

Yes, other immune cells such as B cells, which produce antibodies, undergo hypermutation. This is necessary for generating a diverse range of antibodies to effectively combat a wide range of pathogens. However, other immune cells such as natural killer cells and macrophages do not undergo hypermutation.

5. Are there any potential risks associated with hypermutation?

Yes, there are potential risks associated with hypermutation. As the process involves introducing deliberate mutations into the DNA, there is always a risk of creating harmful mutations that could lead to diseases like cancer. Additionally, hypermutation can also lead to the production of autoantibodies, which can mistakenly attack the body's own cells and tissues.

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