HIV and TCell Numbers/Memory

Bill Lee leew at
Thu Feb 23 12:57:12 EST 1995

In article <kirberg-2302950907380001 at> kirberg at (Jorg Kirberg) writes:
>From: kirberg at (Jorg Kirberg)
>Subject: Re: HIV and TCell Numbers/Memory
>Date: Thu, 23 Feb 1995 08:07:38 GMT

>In article <leew.49.000D1EBC at>, leew at (Bill Lee)

>> In article <3icu9c$1vd at> David Peritt
><Peritt_d at> writes:
>> 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.

>Hi Bill,
>could you give any reason why the expansion must not be Ag mediated ?
>The specificity of the cells is unknown, they are of naive phenotype
>before transfer and gain the memory phenotype. Therefore, why shouldnt
>Ag be responsible for an enormous expansion of certain cells (maybe of
>limited clonal size) whereas the others just stay around, but will be
>difficult to find as outcompeted in cell numbers by the expanding


I think that's a reasonable explanation, although my initial feeling was that 
the failure to find any virgin cells 1 month post-transfer reflected 
polyclonal expansion.  Certainly, the range of environmental Ags which would 
drive proliferation of all cells wouln't be that broad.  Alternative 
explanations, as you correctly point out, would take into account dilution of 
virgin cells by the tremendously expanded population or perhaps death of 
nonstimulated cells leading to selection of the activated population.  Off 
the top of my head I would think that this may be testable as you might 
expect that (or be lucky enough to find) that the expanded pupolation is 
oligoclonal.  If this were so an analysis of TcR repertoires might be 

If a limited expansion (and subsequent selection) were true, what does this 
say about Ag stimulation vis a vis a homeostatic mechanism for obtaining 
"normal" T cell numbers?  To account for that high degree of expansion, 
wouldn't the responding cell have to proliferate much more vigorously to a 
given Ag than it normally would in a normal mouse, to account for the 
increased cellularity in the nude spleen?


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