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Patients infected with HIV have highly variable CD8+ CTL responses despite the high number of circulating CD8+ T cells, an observation that remains poorly understood. In March Journal of Immunology Mohammed Garba and colleagues from University of North Carolina, Chapel Hill, USA, show that the failure of CD8+ T cell responses can be the result of an active HIV regulatory process mediated by secretion of TGF-β1, rather than the absence of CD8+ cells.Garba et al. used flow cytometric methods

Written byTudor Toma
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Patients infected with HIV have highly variable CD8+ CTL responses despite the high number of circulating CD8+ T cells, an observation that remains poorly understood. In March Journal of Immunology Mohammed Garba and colleagues from University of North Carolina, Chapel Hill, USA, show that the failure of CD8+ T cell responses can be the result of an active HIV regulatory process mediated by secretion of TGF-β1, rather than the absence of CD8+ cells.

Garba et al. used flow cytometric methods and measured intracellular cytokines such as TGF-β1 and IFN-γ in lymphocytes from HIV+ donors. They found that numerous HIV proteins or peptides could induce in vitro TGF-β1 secretion by CD8+T cells that is capable of inhibiting the IFN-γ response to HIV and other unrelated vaccinia virus proteins (J Immunol 2002, 168:2247-2254).

These results show a new mechanism by which an HIV-specific response can nonspecifically suppress both HIV and other immune ...

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