IL-2 Immunotherapy to Recently HIV-1 Infected Adults Maintains the Numbers of IL-17 Expressing CD4+ T (TH17) Cells in the Periphery |
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Authors: | Lishomwa C. Ndhlovu Elizabeth Sinclair Lorrie Epling Qi Xuan Tan Terence Ho Aashish R. Jha Ijeoma Eccles-James Camilla Tincati Jay A. Levy Douglas F. Nixon Frederick M. Hecht Jason D. Barbour |
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Affiliation: | 1. Division of Experimental Medicine, Department of Medicine, San Francisco General Hospital, University of California, San Francisco, San Francisco, CA, USA 3. General Clinical Research Center, Department of Medicine, San Francisco General Hospital, University of California, San Francisco, San Francisco, CA, USA 4. Core Immunology Laboratory, Department of Medicine, San Francisco General Hospital, University of California, San Francisco, San Francisco, CA, USA 2. Department of Medicine, San Francisco General Hospital, University of California, San Francisco, San Francisco, CA, USA
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Abstract: | Little is known about the manipulation of IL-17 producing CD4+ T cells (TH17) on a per-cell basis in humans in vivo. Previous studies on the effects of IL-2 on IL-17 secretion in non-HIV models have shown divergent results. We hypothesized that IL-2 would mediate changes in IL-17 levels among recently HIV-1-infected adults receiving anti-retroviral therapy. We measured cytokine T cell responses to CD3/CD28, HIV-1 Gag, and CMV pp65 stimulation, and changes in multiple CD4+ T cell subsets. Those who received IL-2 showed a robust expansion of naive and total CD4+ T cell counts and T-reg counts. However, after IL-2 treatment, the frequency of TH17 cells declined, while counts of TH17 cells did not change due to an expansion of the CD4+ naïve T cell population (CD27+CD45RA+). Counts of HIV-1 Gag-specific T cells declined modestly, but CMV pp65 and CD3/CD28 stimulated populations did not change. Hence, in contrast with recent studies, our results suggest IL-2 is not a potent in vivo regulator of TH17 cell populations in HIV-1 disease. However, IL-2-mediated T-reg expansions may selectively reduce responses to certain antigen-specific populations, such as HIV-1 Gag. |
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