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Department of Pathology, Tokushima University School of Dentistry, Kuramotocho, Tokushima, Japan;
Department of Ophthalmology, Tokyo Dental College, Ichikawa, Chiba, Japan;
Takasago Research Laboratories, Research Institute, Kaneka Co, Takasago, Hyogo, Japan;
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Department of Internal Medicine, Institute of Clinical Medicine, University of Tsukuba, Tsukuba, Ibaraki, Japan;
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Clinical Research Center, National Utano Hospital, Kyoto, Japan;
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Department of Molecular Biology, Osaka Bioscience Institute, Osaka, Japan; and
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Department of Cell Biology, Cancer Institute, Toshima-ku, Tokyo, Japan
Although IL-10 has been implicated in the pathogenesis of several autoimmune diseases, the mechanisms by which this cytokine mediates inflammatory lesions remain to be elucidated. Exocrine gland destruction is an important early step in the development of Sjögren’s syndrome. To better understand the role of IL-10 in Sjögren’s syndrome, we made transgenic mice in which the mouse IL-10 gene was regulated by the human salivary amylase promoter. Transgenic expression of IL-10 induced apoptosis of glandular tissue destruction and lymphocyte infiltration consisting primarily of Fas-ligand (FasL)+ CD4+ T cells, as well as in vitro up-regulation of FasL expression on T cells. These data suggest that overexpression of IL-10 in the glands and their subsequent Fas/FasL-mediated bystander tissue destruction is a causal factor in the development of this disease.
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