title: Human plasmacytoid dendritic cells support Th17 cell effector function in response to TLR7 ligation.
abstract: Signals involved in the commitment of Th17 differentiation are of substantial interest for our understanding of antimicrobial defense mechanisms and autoimmune disorders. Various ways in which myeloid dendritic cells modulate Th17 differentiation have been identified. However, although plasmacytoid dendritic cells (PDCs) are regarded as important players in antiviral/antimicrobial host defense and autoimmune diseases, a putative modulatory role of PDCs in Th17 differentiation has not yet been elucidated in detail. We demonstrated that PDCs are capable of promoting Th17 differentiation in response to TLR7 stimulation. Further, both the differentiation of Th17 cells from naive T cells and the amplification of Th17 effector functions of memory T cells are promoted by PDCs after TLR7 activation. Our data are of strong clinical relevance because TLR7 activation in PDCs might represent one of the missing links between innate and adaptive immune mechanisms and contribute to the amplification of Th17-driven autoimmune disorders as well as viral host defense.
authors.affiliation: Department of Dermatology and Allergy, University Hospital, University of Bonn, Bonn, Germany.
authors.forename: Chun-Feng
authors.initials: CF
authors.lastname: Yu
authors.forename: Wen-Ming
authors.initials: WM
authors.lastname: Peng
authors.forename: Johannes
authors.initials: J
authors.lastname: Oldenburg
authors.forename: Jochen
authors.initials: J
authors.lastname: Hoch
authors.forename: Thomas
authors.initials: T
authors.lastname: Bieber
authors.forename: Andreas
authors.initials: A
authors.lastname: Limmer
authors.forename: Gunther
authors.initials: G
authors.lastname: Hartmann
authors.forename: Winfried
authors.initials: W
authors.lastname: Barchet
authors.forename: Anna Maria
authors.initials: AM
authors.lastname: Eis-Hübinger
authors.forename: Natalija
authors.initials: N
authors.lastname: Novak
mesh_terms: D056704:Adaptive Immunity; D001327:Autoimmune Diseases / Q000276:immunology / Q000378:metabolism; D002454:Cell Differentiation / Q000276:immunology; D002478:Cells, Cultured; D018920:Coculture Techniques; D003713:Dendritic Cells / Q000276:immunology* / Q000378:metabolism* / Q000821:virology; D006801:Humans; D007113:Immunity, Innate; D007156:Immunologic Memory; D018836:Inflammation Mediators / Q000378:metabolism / Q000502:physiology; D007251:Influenza, Human / Q000276:immunology / Q000378:metabolism / Q000821:virology; D020381:Interleukin-17 / Q000096:biosynthesis / Q000502:physiology*; D008024:Ligands; D016192:Resting Phase, Cell Cycle / Q000276:immunology; D006377:T-Lymphocytes, Helper-Inducer / Q000166:cytology / Q000276:immunology* / Q000378:metabolism* / Q000821:virology; D051199:Toll-Like Receptor 7 / Q000378:metabolism* / Q000502:physiology
chemical_list: D018836:Inflammation Mediators; D020381:Interleukin-17; D008024:Ligands; C495348:TLR7 protein, human; D051199:Toll-Like Receptor 7