| γδ T cells enhance autoimmunity by restraining regulatory T cell responses via an interleukin-23-dependent mechanism. | |
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MedLine Citation:
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PMID: 20832339 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Mice that lack interleukin-23 (IL-23) are resistant to T cell-mediated autoimmunity. Although IL-23 is a maturation factor for T helper 17 (Th17) cells, a subset of γδ T cells expresses the IL-23 receptor (IL-23R) constitutively. Using IL-23R reporter mice, we showed that γδ T cells were the first cells to respond to IL-23 during experimental autoimmune encephalomyelitis (EAE). Although γδ T cells produced Th17 cell-associated cytokines in response to IL-23, their major function was to prevent the development of regulatory T (Treg) cell responses. IL-23-activated γδ T cells rendered αβ effector T cells refractory to the suppressive activity of Treg cells and also prevented the conversion of conventional T cells into Foxp3(+) Treg cells in vivo. Thus, IL-23, which by itself has no direct effect on Treg cells, is able to disarm Treg cell responses and promote antigen-specific effector T cell responses via activating γδ T cells. |
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Authors:
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Franziska Petermann; Veit Rothhammer; Malte C Claussen; Jan D Haas; Lorena Riol Blanco; Sylvia Heink; Immo Prinz; Bernhard Hemmer; Vijay K Kuchroo; Mohamed Oukka; Thomas Korn |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2010-09-09 |
Journal Detail:
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Title: Immunity Volume: 33 ISSN: 1097-4180 ISO Abbreviation: Immunity Publication Date: 2010 Sep |
Date Detail:
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Created Date: 2010-09-27 Completed Date: 2010-10-13 Revised Date: 2012-05-07 |
Medline Journal Info:
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Nlm Unique ID: 9432918 Medline TA: Immunity Country: United States |
Other Details:
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Languages: eng Pagination: 351-63 Citation Subset: IM |
Copyright Information:
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Copyright © 2010 Elsevier Inc. All rights reserved. |
Affiliation:
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Klinikum rechts der Isar, Department of Neurology, Technical University Munich, Ismaninger Strasse 22, Munich, Germany. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Amino Acid Sequence Animals Autoimmunity* Encephalomyelitis, Autoimmune, Experimental / etiology Interleukin-17 / biosynthesis Interleukin-23 / physiology* Interleukins / biosynthesis Mice Mice, Inbred C57BL Molecular Sequence Data Receptors, Antigen, T-Cell / physiology Receptors, Antigen, T-Cell, gamma-delta / physiology* Receptors, Interleukin / physiology T-Lymphocytes, Regulatory / immunology* |
| Grant Support | |
ID/Acronym/Agency:
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R01 AI073542-04/AI/NIAID NIH HHS; R01 AI073542-05/AI/NIAID NIH HHS; R01 AI073542-05S1/AI/NIAID NIH HHS; R01 AI073542-06/AI/NIAID NIH HHS; R01 NS030843-19/NS/NINDS NIH HHS; R01AI 073542-03/AI/NIAID NIH HHS; R01NS 30843/NS/NINDS NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Interleukin-17; 0/Interleukin-23; 0/Interleukins; 0/Receptors, Antigen, T-Cell; 0/Receptors, Antigen, T-Cell, gamma-delta; 0/Receptors, Interleukin; 0/interleukin-22; 0/interleukin-23 receptor, mouse |
| Comments/Corrections | |
Comment In:
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Nat Rev Immunol. 2010 Oct;10(10):679
[PMID:
20879167
]
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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