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From the * Howard Hughes Medical Institute, Department of Medicine, National Jewish Medical and
Research Center, Denver, Colorado 80206; Although much is known about the activation, proliferation, and function of CD4+ T cells, little is known about how they survive as resting T cells in animals. Resting T cells have a half-life
in animals of more than a week; however, when they are removed from animals and placed in
tissue culture their half-life falls to ~24 h. In this paper, we show that the survival of resting T
cells in vitro is promoted by two cytokines, interleukins 4 and 7 (IL-4, IL-7). They may do this
in part by maintaining levels of survival-promoting proteins such as Bcl-2 in the cells, because
the levels of Bcl-2 and Bcl-Xl in resting T cells fall rapidly after the cells are isolated from animals, and are maintained by culture in IL-4. Because the IL-4 receptor is known to signal
through the JAK1 and JAK3/Stat6 pathway, we tested whether Stat6 was required for IL-4-
dependent T cell survival. Surprisingly, we found that IL-4 rescued T cells from apoptosis in
what appeared to be a Stat6-independent manner. These results demonstrate that the survival
of resting T cells is an active process that can be affected by signals delivered by cytokines and
also suggest that the IL-4 receptor on resting T cells may use a novel signaling pathway to facilitate T cell viability.
Department of Biochemistry Biophysics and Genetics
and § Departments of Immunology and Medicine, University of Colorado Health Sciences Center,
Denver, Colorado 80206; and the §St. Jude Children's Research Hospital, Memphis, Tennessee 38105
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