21 research outputs found

    The Joint Program Dilemma: Analyzing the Pervasive Role That Social Dilemmas Play in Undermining Acquisition Success

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    Tenth Annual Acquisition Research Symposium Acquisition ManagementExcerpt from the Proceedings of the Tenth Annual Acquisition Research Symposium Acquisition ManagementNaval Postgraduate School Acquisition Research ProgramPrepared for the Naval Postgraduate School, Monterey, CANaval Postgraduate School Acquisition Research ProgramApproved for public release; distribution is unlimited

    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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    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+ naĂŻve 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

    The Decline and Fall of Joint Acquisition Programs

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    Naval Postgraduate School Acquisition Research Progra
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