[HTML][HTML] Dendritic Cells from HIV Controllers Have Low Susceptibility to HIV-1 Infection In Vitro but High Capacity to Capture HIV-1 Particles

C Hamimi, A David, P Versmisse, L Weiss, T Bruel… - PLoS …, 2016 - journals.plos.org
C Hamimi, A David, P Versmisse, L Weiss, T Bruel, D Zucman, V Appay, A Moris…
PLoS One, 2016journals.plos.org
HIV controllers (HICs), rare HIV-1 infected individuals able to control viral replication without
antiretroviral therapy, are characterized by an efficient polyfunctional and cytolytic HIV-
specific CD8+ T cell response. The mechanisms underlying the induction and maintenance
of such response in many HICs despite controlled viremia are not clear. Dendritic cells play
a crucial role in the generation and reactivation of T cell responses but scarce information is
available on those cells in HICs. We found that monocyte derived dendritic cells (MDDCs) …
HIV controllers (HICs), rare HIV-1 infected individuals able to control viral replication without antiretroviral therapy, are characterized by an efficient polyfunctional and cytolytic HIV-specific CD8+ T cell response. The mechanisms underlying the induction and maintenance of such response in many HICs despite controlled viremia are not clear. Dendritic cells play a crucial role in the generation and reactivation of T cell responses but scarce information is available on those cells in HICs. We found that monocyte derived dendritic cells (MDDCs) from HICs are less permissive to HIV-1 infection than cells from healthy donors. In contrast MDDCs from HICs are particularly efficient at capturing HIV-1 particles when compared to cells from healthy donors or HIV-1 patients with suppressed viral load on antiretroviral treatment. MDDCs from HICs expressed on their surface high levels of syndecan-3, DC-SIGN and MMR, which could cooperate to facilitate HIV-1 capture. The combination of low susceptibility to HIV-1 infection but enhanced capacity to capture particles might allow MDDCs from HICs to preserve their function from the deleterious effect of infection while facilitating induction of HIV-specific CD8+ T cells by cross-presentation in a context of low viremia.
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