HIV and TCell Numbers/Memory

Bill Lee leew at
Tue Feb 21 13:07:06 EST 1995

In article <3icu9c$1vd at> David Peritt <Peritt_d at> writes:
>From: David Peritt <Peritt_d at>
>Subject: Re: HIV and TCell Numbers/Memory
>Date: 21 Feb 1995 14:45:00 GMT

>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

Our experience:  We separated normal CD4 cells into virgin and memory 
populations on the basis of CD45RB expression.  These cells were transferred 
into BALB/c nu/nu mice.  4 weeks post-transfer, there were increased numbers 
of CD4 cells in both groups of mice.  However, the mioce which initially 
received phenotypically virgin cells had greater expansion (13x) as compared 
to the mice that received phenotypically memory cells (3.5x) (both averaged 
over 10 different transfers).  In terms of raw numbers, whereas mice which 
received memory cells and nude mice with no transferred cells had a relatively 
low number of splenocytes (including T cells (1-4 x 10 (7) if I remember 
correctly) the mice with transferred virgin cells had a cellularity of 1-2 x 
10(8) or about what you would expect from a normal BALB/c mouse.  Regardless 
of which population was transferred the phenotype was always that of a memory 
cell (Bell and Sparshott expts notwithstanding, although I think that data 
comes from long-term (1-year) transfers).  This is interesting as the change 
in virgin phenotype must not be due to activation by Ag but due to expansion 
as part of homeostasis.  Also, again if my memory serves, maintenance of 
either transferred population seemed to require co-immunization at the time of 
transfer.  This was not Ag dependent; CFA alone would do as well.  What this 
means I don't know.


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