HIV and TCell Numbers/Memory

David Peritt Peritt_d at a1.mscf.upenn.edu
Tue Feb 21 09:45:00 EST 1995


In article <ralph.1143705994A at news.arizona.edu> Ralph M Bernstein,
ralph at ccit.arizona.edu writes:
>question: where the hell are those tcell being made?  everyone knows that
>aafter or at puberty the thymus involudes-we are left with a very poor
>education system.  w/out the thymic education we run the risk of
>autoimmunity/ect.  so what goes on here?  it cannot be tcells that
havenot
>encountered antigen in the perhiphery, since they die in around 72h after
>release if they dont encounter ag.  evenbetter, i dont think it could be
>from expanding memory cells because they would be infected any way-like a
>roachmotel, in hiv infected lymphnodes, tcells go in but they dont go
out.  


It is surmized with little data that peripheral T cells expand to fill
the void.  There is little evidence for extrathymic generation of new T
cells (except for those gut g/d cells).  Whether it is naive or memory T
expanding is unknown to me.  What I am saying is that I do not think it
is known but yes it is a very basic immunology question.  In fact, the
reason I posted the homeostasis question was partially due to your
question.  If peripheral T's are proliferating they must get a signal to
do so when T levels drop.  What may that be????  This question could be
answered by someone with nimble fingers willing to do the proper Tx
experiments of naive and memory T in athymic mice.   You put different
amount of T in and see who proliferates to compensate.  It may have been
done but us human Immunologist never get to do many Tx exps and therefore
never read these papers which can be done so elegantly partially out of
jeolousy.



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