Abstract
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.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Arthritis, Experimental / blood
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Arthritis, Experimental / complications
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Arthritis, Experimental / immunology*
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Arthritis, Experimental / pathology*
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Cartilage / metabolism
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Cartilage / pathology
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Cell Differentiation
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Inflammation / blood
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Inflammation / complications
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Inflammation / pathology
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Inflammation Mediators / metabolism
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Integrases / metabolism
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Joints / pathology
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Lymphocyte Specific Protein Tyrosine Kinase p56(lck) / metabolism
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Matrix Metalloproteinase 3 / blood
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Mice
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Mice, Inbred C57BL
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Mice, Knockout
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Receptors, Aryl Hydrocarbon / deficiency*
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Receptors, Aryl Hydrocarbon / metabolism
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T-Lymphocytes / metabolism*
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Th17 Cells / immunology
Substances
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Inflammation Mediators
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Receptors, Aryl Hydrocarbon
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Lymphocyte Specific Protein Tyrosine Kinase p56(lck)
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Cre recombinase
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Integrases
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Matrix Metalloproteinase 3