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CUTTING EDGE |
*
Department of Pediatrics, National Jewish Medical and Research Center, Denver, CO 80206;
Departments of Immunology, Pediatrics, and Biochemistry and Molecular Genetics, University of Colorado Health Sciences Center, Denver, CO 80262
In early HIV disease, immunodeficiency is characterized by the
inability of CD4+ T cells to produce a critical
cytokine, IL-2, and to express the receptor for IL-2 (IL-2R) in
response to antigenic or mitogenic stimulation. The shared common
-chain (c) of IL-2R and its associated Janus kinase,
JAK3, are indispensable for normal T cell function. Here, we show that
the inhibition of IL-2R expression and proliferation induced by
ligation of CD4 by HIV envelope glycoprotein, gp120, is correlated with
inhibition of expression and activation of JAK3. Stimulation through
the c-related cytokine receptors restores JAK3
expression and activation and rescues CD4-mediated T cell
unresponsiveness. Collectively, these data argue that inhibition of
JAK3 expression and activation may, in part, explain the T cell
dysfunction seen in early HIV disease. In addition, rescue from
gp120-mediated T cell unresponsiveness by activation of JAK3 suggests a
novel therapeutic approach for enhancing immune function in HIV
disease.
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