Re:CRISPR eliminates HIV-1 infection in live animals
by furiens on Thursday May 04, 2017 @09:21AM
(#14264582)
Also google "somatic hypermutation". That multiplication process for B cells is inexact, and introduces mutations into the DNA (and therefore structure) of its children. There's a process which indicates whether any of these new antibodies binds better than the original one, which becomes a new candidate for multiplying.
There's fairly recent technology to sequence these antibodies en masse, which gives you a whole load (~10^6) of these antibody DNA sequences. It's a fascinating and frustrating exercise to try and reconstruct the mutation history and families of related cells from this data.
Re:CRISPR eliminates HIV-1 infection in live animals
by lr4444lr on Wednesday May 03, 2017 @08:35AM
(#14255105)
Is there concern that those long-lived antibody clones become pathological themselves?
Re:CRISPR eliminates HIV-1 infection in live animals
by virusduck on Wednesday May 03, 2017 @11:39AM
(#14256674)
Yes and no. Yes in that some of the many billions of combinations of antibody genes can recognize self proteins, which is a problem. However, during maturation of B cells, the immune system has a mechanism for killing of those B cells which would produce anti-self antibodies before they mature. There are times when this fails to work--think Grave's Disease, many forms of lupus, alopecia, etc.
I think in the sense you are asking, though, is that any long-lived plasma cell or memory B cell that is active will probably not change to the extent that they would attack self. I don't know off the top of my head if there are examples of this, but I can't think of any.
There are actually two separate systems: the T cells and B cells. I recommend the very readable Lauren Sompayrac's "How the Immune System Works". Or google/wiki "clonal selection" and "VDJ recombination".