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,§,¶,
,¶
*
Howard Hughes Medical Institute,
Department of Immunology, National Jewish Medical and Research Center, and Departments of
Biochemistry and Molecular Genetics,
§
Pharmacology, and
¶
Medicine, University of Colorado Medical School, Denver, CO 80207
Older humans and mice frequently contain very large clones of
CD8+ T cells. In mice these cells are phenotypically very
similar to memory CD8+ T cells. Like memory
CD8+ T cells, most members of the clones are in continuous
slow division, apparently independently of Ag stimulation.
Proliferation of the CD8+ clonal T cells is inhibited in
mice treated with Ab to the IL-2R 
-chain that blocks signaling by
either IL-2 or IL-15. However, inhibition of IL-2 increases the numbers
of dividing clonal cells. Therefore, like normal memory
CD8+ T cells, expansion of the clones is driven by IL-15
and inhibited by IL-2 and is probably limited by the amounts of IL-15
and IL-2 present in the host. Control by these two cytokines may
account for the fact that, although the clones can be very large, they
do not overwhelm or kill their hosts. Nevertheless the clonal cells
compete successfully with normal memory CD8+ T cells for
growth. Perhaps the clonal cells use IL-15 more effectively or are more
resistant to the inhibitory effects of IL-2. Thus they might affect the
immune response of their hosts by competing for factors that stimulate
and inhibit normal CD8+ memory T
cells.
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