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Defective Dendritic Cell Function in HIV-Infected Patients Receiving Effective Highly Active Antiretroviral Therapy: Neutralization of IL-10 Production and Depletion of CD4⁺CD25⁺ T Cells Restore High Levels of HIV-Specific CD4⁺ T Cell Responses Induced by Dendritic Cells Generated in the Presence of IFN-¹

Cédric Carbonneil^*, Vladimira Donkova-Petrini^*, Albertine Aouba and Laurence Weiss^2,*,,

^* Institut National de la Santé et de la Recherche Médicale Unité 430, Institut des Cordeliers, Université René Descartes, and Hôpital Européen Georges Pompidou, Paris, France

We previously demonstrated that GM-CSF/IFN- combination allowed the differentiation of monocytes from HIV-infected patients into dendritic cells (DCs) exhibiting high CD8⁺ T cell stimulating abilities. The present study was aimed at characterizing the ability of DCs generated in the presence of GM-CSF and IFN- to induce CD4 T cell responses. DCs were generated from monocytes of HIV-infected patients in the presence of GM-CSF with either IFN- (IFN-DCs) or IL-4 (IL-4-DCs) for 7 days. Eleven patients receiving highly active antiretroviral therapy and exhibiting CD4 cell counts above 400/mm³ and plasma HIV-RNA <50 copies/ml for at least 1 year were included in the study. Both DC populations were found to be defective in inducing autologous (in response to tuberculin or HIV-p24) or allogeneic CD4 T cell proliferation. Neutralization of IL-10 during the differentiation of IFN-DCs, but not during the DC-T cell coculture, significantly increased their ability to stimulate autologous CD4 T cell proliferation in response to tuberculin and allogeneic CD4 T cell proliferation (4.1-fold and 3.0-fold increases, respectively, at the DC to T cell ratio of 1:10). Moreover, IL-10 neutralization and CD4⁺CD25⁺ T cell depletion synergistically act to dramatically increase HIV-p24-specific CD4 T cell responses induced by IFN-DCs (31.7-fold increase) but not responses induced by IL-4-DCs. Taken together, our results indicate that IFN-DCs are more efficient than IL-4-DCs to stimulate CD4⁺ T cell proliferation, further supporting their use for immune-based therapy in HIV infection.

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