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

Doris Wilflingseder 1 Andrea Schroll 1 Hubert Hackl 1 Ralf Gallasch 1 Dan Frampton 2, 3 Cornelia Lass-Flörl 1 Gianfranco Pancino 4 Zlatko Trajanoski 5 Asier Saez-Cirion 6 Olivier Lambotte 7, 8, 9 Laurence Weiss 10, 4 Paul Kellam 3, 2 Teunis Geijtenbeek 5 Günter Weiss 1 Wilfried Posch 1
1 IMU - Innsbruck Medical University [Austria]
2 UCL - University College of London [London]
3 Wellcome Trust Genome Campus
4 Régulation des Infections Rétrovirales
5 AMC - Academic Medical Center - Academisch Medisch Centrum [Amsterdam]
6 HIV, Inflammation et persistance
7 APHP, Service de Médecine Interne-Immunologie Clinique, Hôpitaux Universitaires Paris Sud
8 UP11 UFR Médecine - Université Paris-Sud 11 - Faculté de médecine
9 Régulation de la réponse immune, infection VIH-1 et autoimmunité
10 HEGP - Hôpital Européen Georges Pompidou [APHP]
Abstract : 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.
Keywords : HIV-1 Dendritic Cells Female Adult Antigens CD11b CD11c Cell Differentiation complement Complement System Proteins Humans Male MAPK Middle Aged opsonization Th17 Th17 Cells
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Article dans une revue
The Journal of Infectious Diseases, 2015, 212 (1), pp.44--56. 〈10.1093/infdis/jiv014〉
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Doris Wilflingseder, Andrea Schroll, Hubert Hackl, Ralf Gallasch, Dan Frampton, et al.. Immediate T-Helper 17 Polarization Upon Triggering CD11b/c on HIV-Exposed Dendritic Cells. The Journal of Infectious Diseases, 2015, 212 (1), pp.44--56. 〈10.1093/infdis/jiv014〉. 〈pasteur-01420413〉

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