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© Charles Dauguet
Virus VIH-2, second virus du sida isolé en 1985 par l'équipe du Pr. Montagnier de l'Institut Pasteur.
Publication : The Journal of infectious diseases

Immediate T-Helper 17 Polarization Upon Triggering CD11b/c on HIV-Exposed Dendritic Cells

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in The Journal of infectious diseases - 12 Jan 2015

Wilflingseder D, Schroll A, Hackl H, Gallasch R, Frampton D, Lass-Flörl C, Pancino G, Saez-Cirion A, Lambotte O, Weiss L, Kellam P, Trajanoski Z, Geijtenbeek T, Weiss G, Posch W

Link to Pubmed [PMID] – 25583169

J. Infect. Dis. 2015 Jul;212(1):44-56

Early on in human immunodeficiency virus (HIV) type 1 infection, gut T-helper (Th) 17 cells are massively depleted leading eventually to compromised intestinal barrier function and excessive immune activation. In contrast, the functional Th17 cell compartment of the gut is well-maintained in nonpathogenic simian immunodeficiency virus infection as well as HIV-1 long-term nonprogressors. Here, we show that dendritic cells (DCs) loaded with HIV-1 bearing high surface complement levels after incubation in plasma from HIV-infected individuals secreted significantly higher concentrations of Th17-polarizing cytokines than DCs exposed to nonopsonized HIV-1. The enhanced Th17-polarizing capacity of in vitro-generated and BDCA-1(+) DCs directly isolated from blood was linked to activation of ERK. In addition, C3a produced from DCs exposed to complement-opsonized HIV was associated with the higher Th17 polarization. Our in vitro and ex vivo data, therefore, indicate that complement opsonization of HIV-1 strengthens DC-mediated antiviral immune functions by simultaneously triggering Th17 expansion and intrinsic C3 formation via DC activation.

http://www.ncbi.nlm.nih.gov/pubmed/25583169