| C5a receptor signalling in dendritic cells controls the development of maladaptive Th2 and Th17 immunity in experimental allergic asthma. | |
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MedLine Citation:
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PMID: 23212198 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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The pathways underlying dendritic cell (DC) activation in allergic asthma are incompletely understood. Here we demonstrate that adoptive transfer of ovalbumin-pulsed wild-type (wt) but not of C5a receptor-deficient (C5aR(-/-)) bone marrow (BM)-derived DCs (BMDCs) induced mixed T helper type 2 (Th2)/Th17 maladaptive immunity, associated with severe airway hyperresponsiveness, mucus production, and mixed eosinophilic/neutrophilic inflammation. Mechanistically, antigen uptake, processing, and CD11b expression were reduced in C5aR(-/-) BMDCs. Further, interleukin (IL)-1β, -6, and -23 production were impaired resulting in reduced Th17 cell differentiation, associated with accelerated activated T-cell death in vitro and in vivo. Surprisingly, we found an increased frequency of CD11b(hi)CD11c(int)Gr1(+)F4/80(+) cells, expressing arginase and nitric oxide synthase in C5aR(-/-) BM preparations. Intratracheal administration of ovalbumin-pulsed wt DCs and sorted CD11b(hi)CD11c(int)Gr1(+)F4/80(+) C5aR(-/-) cells reduced Th2 immune responses in vivo. Together, we uncover novel roles for C5aR in Th17 differentiation, T-cell survival, and differentiation of a DC-suppressor population controlling Th2 immunity in experimental allergic asthma.Mucosal Immunology advance online publication 5 December 2012; doi:10.1038/mi.2012.119. |
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Authors:
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I Schmudde; H A Ströver; T Vollbrandt; P König; C M Karsten; Y Laumonnier; J Köhl |
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Publication Detail:
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Type: JOURNAL ARTICLE Date: 2012-12-05 |
Journal Detail:
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Title: Mucosal immunology Volume: - ISSN: 1935-3456 ISO Abbreviation: Mucosal Immunol Publication Date: 2012 Dec |
Date Detail:
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Created Date: 2012-12-5 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 101299742 Medline TA: Mucosal Immunol Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Affiliation:
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Institute for Systemic Inflammation Research, University of Lübeck, Lübeck, Germany. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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