Abstract
T cell death-associated gene 8 (TDAG8) is a G-protein-coupled receptor identified by differential mRNA display during thymocyte apoptosis induced by T cell receptor engagement. To examine the physiological role of an orphan G-protein-coupled receptor TDAG8 in inflammation, we studied various immune-mediated inflammatory disease models using TDAG8-deficient mice. We found that TDAG8-deficient mice showed significant exacerbation of anti-type II collagen antibody-induced arthritis and delayed-type hypersensitivity, and showed a slight exacerbation of collagen-induced arthritis. These results suggest that TDAG8 acts as a negative regulator of inflammation.
Copyright © 2011 Elsevier B.V. All rights reserved.
MeSH terms
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Animals
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Antibodies / immunology
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Antibodies / pharmacology
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Arthritis, Experimental / chemically induced
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Arthritis, Experimental / immunology
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Arthritis, Experimental / metabolism
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Cattle
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Collagen Type II / immunology
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Collagen Type II / pharmacology
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Gene Knockout Techniques
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Hypersensitivity, Delayed / immunology
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Hypersensitivity, Delayed / metabolism
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Inflammation / immunology
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Inflammation / metabolism
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Inflammation / pathology
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Male
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Methylation
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Mice
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Mice, Inbred C57BL
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Receptors, G-Protein-Coupled / deficiency
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Receptors, G-Protein-Coupled / genetics
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Receptors, G-Protein-Coupled / metabolism
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Serum Albumin, Bovine / metabolism
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T-Lymphocytes / immunology
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T-Lymphocytes / metabolism
Substances
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Antibodies
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Collagen Type II
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GPR65 protein, mouse
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Receptors, G-Protein-Coupled
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Serum Albumin, Bovine