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Departments of
*
Medicine and
Microbiology and Immunology, and
Emory Vaccine Center, Emory University School of Medicine, Atlanta, GA 30322;
Department of Biochemistry, University of Urbino, Urbino, Italy;
¶ Division of Infectious Diseases, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390;
|| Department of Public Health, University of Messina, Messina, Italy; and
# Department of Internal Medicine, University Politecnica delle Marche, Ancona, Italy
The immunodeficiency that follows HIV infection is related to the virus-mediated killing of infected CD4+ T cells, the chronic activation of the immune system, and the impairment of T cell production. In this study we show that in HIV-infected individuals the loss of IL-7R (CD127) expression defines the expansion of a subset of CD8+ T cells, specific for HIV as well as other Ags, that show phenotypic (i.e., loss of CCR7 and CD62 ligand expression with enrichment in activated and/or proliferating cells) as well as functional (i.e., production of IFN-
, but not IL-2, decreased ex vivo proliferative potential and increased susceptibility to apoptosis) features of effector T cells. Importantly, in HIV-infected individuals the levels of CD8+CD127– T cells are directly correlated with the main markers of disease progression (i.e., plasma viremia and CD4+ T cell depletion) as well as with the indices of overall T cell activation. In all, these results identify the expansion of CD8+CD127– effector-like T cells as a novel feature of the HIV-associated immune perturbation. Further studies are thus warranted to determine whether measurements of CD127 expression on CD8+ T cells may be useful in the clinical management of HIV-infected individuals.
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