| Aryl hydrocarbon receptor deficiency in T cells suppresses the development of collagen-induced arthritis. | |
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MedLine Citation:
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PMID: 21825138 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The contributions of aryl hydrocarbon receptor (Ahr) to the pathogenesis of rheumatoid arthritis have not been elucidated. Here, we show that Ahr deficiency ameliorated collagen-induced arthritis, a mouse model of RA. Collagen-immunized Ahr KO mice showed decreased serum levels of such proinflammatory cytokines as IL-1β and IL-6. The Th17 and Th1 cell populations in lymph nodes from these mice decreased and increased, respectively, whereas the percentage of regulatory T cells was unchanged. Interestingly, a lack of Ahr specifically in T cells significantly suppressed collagen-induced arthritis development, whereas Ahr deficiency in macrophages had no effect. These finding indicate that the development of experimental autoimmune arthritis depends on the presence of Ahr in T cells, and that Th1/Th17 balance may be particularly important for this process. |
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Authors:
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Taisuke Nakahama; Akihiro Kimura; Nam Trung Nguyen; Ichino Chinen; Hamza Hanieh; Keiko Nohara; Yoshiaki Fujii-Kuriyama; Tadamitsu Kishimoto |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2011-08-08 |
Journal Detail:
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Title: Proceedings of the National Academy of Sciences of the United States of America Volume: 108 ISSN: 1091-6490 ISO Abbreviation: Proc. Natl. Acad. Sci. U.S.A. Publication Date: 2011 Aug |
Date Detail:
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Created Date: 2011-08-29 Completed Date: 2011-10-27 Revised Date: 2012-02-23 |
Medline Journal Info:
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Nlm Unique ID: 7505876 Medline TA: Proc Natl Acad Sci U S A Country: United States |
Other Details:
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Languages: eng Pagination: 14222-7 Citation Subset: IM |
Affiliation:
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Laboratory of Immune Regulation, Osaka University World Premier International Immunology Frontier Research Center, Osaka 565-0871, Japan. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Arthritis, Experimental / blood, complications, immunology*, pathology* Cartilage / metabolism, pathology Cell Differentiation Inflammation / blood, complications, pathology Inflammation Mediators / metabolism Integrases / metabolism Joints / pathology Lymphocyte Specific Protein Tyrosine Kinase p56(lck) / metabolism Matrix Metalloproteinase 3 / blood Mice Mice, Inbred C57BL Mice, Knockout Receptors, Aryl Hydrocarbon / deficiency*, metabolism T-Lymphocytes / metabolism* Th17 Cells / immunology |
| Chemical | |
Reg. No./Substance:
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0/Inflammation Mediators; 0/Receptors, Aryl Hydrocarbon; EC 2.7.10.2/Lymphocyte Specific Protein Tyrosine Kinase p56(lck); EC 2.7.7.-/Cre recombinase; EC 2.7.7.-/Integrases; EC 3.4.24.17/Matrix Metalloproteinase 3 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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