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J Clin Invest ; 122(12): 4685-97, 2012 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-23160198

RESUMO

Acute HIV-1 infection results in dysregulated immunity, which contributes to poor control of viral infection. DCs are key regulators of both adaptive and innate immune responses needed for controlling HIV-1, and we surmised that factors elicited during acute HIV-1 infection might impede DC function. We derived immature DCs from healthy donor peripheral blood monocytes and treated them with plasma from uninfected control donors and donors with acute HIV-1 infections. We found that the plasma from patients with HIV specifically inhibited DC function. This suppression was mediated by elevated apoptotic microparticles derived from dying cells during acute HIV-1 infection. Apoptotic microparticles bound to and inhibited DCs through the hyaluronate receptor CD44. These data suggest that targeting this CD44-mediated inhibition by apoptotic microparticles could be a novel strategy to potentiate DC activation of HIV-specific immunity.


Assuntos
Apoptose , Micropartículas Derivadas de Células/imunologia , Células Dendríticas/imunologia , Infecções por HIV/imunologia , HIV-1/imunologia , Receptores de Hialuronatos/metabolismo , Micropartículas Derivadas de Células/virologia , Células Dendríticas/fisiologia , Células Dendríticas/virologia , Infecções por HIV/sangue , HIV-1/fisiologia , Humanos , Receptores de Hialuronatos/fisiologia , Imunidade Inata , Receptores Toll-Like/metabolismo , Viremia/virologia
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