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1
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Lymphocyte Cell Biology Section, National Institute of Arthritis and Musculoskeletal and Skin Diseases,
Laboratory of Immune Cell Biology, National Cancer Institute,
Pediatric Endocrinology Branch, National Institute of Child Health and Human Development, and
Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892
Despite the effects of glucocorticoids on immune function,
relatively little is known about glucocorticoid-inducible genes and how
their products may regulate lymphocyte function. Using DNA microarray
technology to analyze gene expression in PBMC from healthy donors, we
identified IL-7R
as a glucocorticoid-inducible gene. This
observation was confirmed at the mRNA and protein levels. Conversely,
TCR signaling decreased IL-7R expression, and the relative strength
of signaling between these two receptors determined the final IL-7R
levels. The up-regulation of IL-7R by glucocorticoids was associated
with enhanced IL-7-mediated signaling and function. Moreover,
IL-7-mediated inhibition of apoptosis at increasing concentrations of
glucocorticoids is consistent with enhanced cell sensitivity to IL-7
following glucocorticoid exposure. These observations provide a
mechanism by which glucocorticoids may have a positive influence on T
cell survival and function.
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