Innate signaling in HIV-1 infection of dendritic cellsvan der Vlist, Michiel; van der Aar, Angelic M.G.; Gringhuis, Sonja I.; Geijtenbeek, Teunis B.H.Current Opinion in HIV & AIDS: September 2011 - Volume 6 - Issue 5 - p 348–352 doi: 10.1097/COH.0b013e328349a2d1 Innate immunity: Edited by William A. Paxton and Teunis B.H. Geijtenbeek Abstract Author Information Abstract Purpose of review: This review summarizes the current knowledge of innate signaling events that are involved in HIV-1 infection. We here focus on dendritic cells, which are among the first cells that encounter HIV-1 after exposure. Recent findings: HIV-1 triggers multiple pattern recognition receptors on dendritic cells that facilitate infection and transmission to T cells. Triggering of the C-type lectin DC-SIGN induces signals that promote HIV-1 replication in dendritic cells and transmission to T cells. Similarly, dendritic cell immunoreceptor has been shown to bind HIV-1 and facilitate transmission to T cells. The cytosolic sensors TRIM5 and cyclophilin A recognize capsid proteins and activate antiviral responses to prevent HIV-1 infection. Moreover, activation of mammalian target of rapamycin (mTOR) by HIV downregulates autophagy preventing adaptive immune responses. Summary: Dendritic cells express an array of pattern recognition receptors that are involved in HIV-1 infection. However, HIV-1 dampens signaling by these receptors leading to suppressed responses or takes advantage of their signaling for its own benefit. Author Information Center for Experimental and Molecular Medicine and Center for Infection and Immunity Amsterdam, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands Correspondence to Teunis B.H. Geijtenbeek, Center for Experimental and Molecular Medicine and Center for Infection and Immunity Amsterdam, Academic Medical Center, University of Amsterdam, Meibergdreef 9, 1105 AZ Amsterdam, The NetherlandsTel: +31 205 666 309; fax: +31 206 977 192; e-mail: T.B.Geijtenbeek@amc.uva.nl © 2011 Lippincott Williams & Wilkins, Inc.