| Human slan (6-sulfo LacNAc) dendritic cells are inflammatory dermal dendritic cells in psoriasis and drive strong T(h)17/T(h)1 T-cell responses. | |
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MedLine Citation:
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PMID: 21377044 Owner: NLM Status: In-Data-Review |
Abstract/OtherAbstract:
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BACKGROUND: Psoriasis is a chronic inflammatory skin disease that is considered to result from activated T cells stimulated by a population of inflammatory dermal dendritic cells (DCs). The origin and identity of these inflammatory dermal DCs are largely unknown. OBJECTIVE: We previously identified slanDCs (6-sulfo LacNAc) DCs as a rich source of TNF-α and as the early major source of IL-12. Here we studied the relevance of slanDCs as inflammatory dermal DCs in psoriasis. METHODS: Psoriasis skin samples were stained for the presence of activated slanDCs. Functional studies were carried out to determine the cytokine production of slanDCs, their T(h)17/T(h)1 T-cell programming, and their migration behavior. RESULTS: Large numbers of IL-23, TNF-α, and inducible nitric oxide synthase expressing slanDCs were found in psoriatic skin samples, which can be recruited by C5a, CX3CL1, and CXCL12. SlanDCs isolated from blood produced high levels of IL-1ß, IL-23, IL-12, and IL-6. Compared with classic CD1c(+) DCs, slanDCs were far more powerful in programming T(h)17/T(h)1 T cells that secrete IL-17, IL-22, TNF-α, and IFN-γ, yet CD1c(+) DCs induced a higher IL-10 production of T cells. Self-nucleic acids complexed to cathelicidin LL37 trigger endosomal Toll-like receptor (TLR) signaling (TLR7, TLR8, TLR9) and are key factors for the activation of DCs in psoriasis. We show that slanDCs respond particularly well to complexes formed of self-RNA and LL37. Similarly, slanDCs stimulated with a synthetic TLR7/8 ligand produced high levels of proinflammatory cytokines. CONCLUSION: Our study defines slanDCs as inflammatory dermal DCs in psoriasis and identifies their strong capacity to induce T(h)17/T(h)1 responses. |
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Authors:
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Anja Hänsel; Claudia Günther; Jens Ingwersen; Josephine Starke; Marc Schmitz; Michael Bachmann; Michael Meurer; Ernst Peter Rieber; Knut Schäkel |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: The Journal of allergy and clinical immunology Volume: 127 ISSN: 1097-6825 ISO Abbreviation: J. Allergy Clin. Immunol. Publication Date: 2011 Mar |
Date Detail:
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Created Date: 2011-03-07 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 1275002 Medline TA: J Allergy Clin Immunol Country: United States |
Other Details:
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Languages: eng Pagination: 787-794.e9 Citation Subset: AIM; IM |
Copyright Information:
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Copyright © 2011 American Academy of Allergy, Asthma & Immunology. Published by Mosby, Inc. All rights reserved. |
Affiliation:
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Institute of Immunology, Faculty of Medicine, Technical University of Dresden, Dresden, Germany; Department of Dermatology, University Hospital, Heidelberg, Germany. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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