Abstract
HIV disease results in decreased IL-7 receptor expression and IL-7 responsiveness in T cells. To explore mechanisms of these deficiencies, we compared CD127 expression and IL-7 induction of P-STAT5 in T cells from HIV-infected persons with serum concentrations of cytokines (IL-7, IL-6 and IL-15), markers of microbial translocation (sCD14 and LPS), and with an indicator of oxidative stress (malondialdehyde (MDA) adducts). CD127 expression was directly related to IL-7 responsiveness in most CD8+ T cell subsets but not in CD4+ T cells from HIV-infected persons. MDA adducts were increased in serum of HIV-infected patients and were inversely related to IL-7 responsiveness in CD8+ T cells and in central memory CD4+ T cells. Incubation of T cells from healthy controls with hydrogen peroxide resulted in impairments in IL-7 induction of P-STAT5. These findings suggest that oxidative stress that is characteristic of HIV disease could contribute to impairments in IL-7 responsiveness and disrupt T cell homeostasis.
Highlights
IL-7 is an important cytokine for immune system homeostasis
To assess IL-7 responsiveness in T cell subsets, peripheral blood mononuclear cells (PBMC) were stimulated with rIL-7 and P-STAT5 was measured by intracellular flow cytometry
It is well established that T cells from HIV-infected persons respond less readily to IL-7 stimulation than cells from healthy controls [5,11,12,13,30]
Summary
IL-7 is an important cytokine for immune system homeostasis. IL-7 promotes T cell survival and mediates homeostatic proliferation in lymphopenic conditions [1,2,3]. T cells from HIV-infected persons tend to display poor intracellular signaling responses to IL-7 stimulation, as measured by phosphorylation of STAT-5 [5,11,12,13]. These perturbations in IL-7 responsiveness could contribute to HIV pathogenesis and adversely affect T cell reconstitution during administration of anti-retroviral therapy. Both IL-7-induced P-STAT5 signaling and CD127 receptor expression have been linked to T cell recovery during anti-retroviral therapy administration [14,15,16,17]
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