TY - JOUR
T1 - Fas ligand-mediated exocrinopathy resembling Sjogren's syndrome in mice transgenic for IL-10
AU - Saito, Ichiro
AU - Haruta, Kumiko
AU - Shimuta, Misa
AU - Inoue, Hiroko
AU - Sakurai, Hiroshi
AU - Yamada, Koichi
AU - Ishimaru, Naozumi
AU - Higashiyama, Hiroyuki
AU - Sumida, Takayuki
AU - Ishida, Hiroshi
AU - Suda, Takashi
AU - Noda, Tetsuo
AU - Hayashi, Yoshio
AU - Tsubota, Kazuo
N1 - Copyright:
Copyright 2007 Elsevier B.V., All rights reserved.
PY - 1999/3/1
Y1 - 1999/3/1
N2 - 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 Sjogren's syndrome. To better understand the role of IL-10 in Sjogren'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 upregulation 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.
AB - 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 Sjogren's syndrome. To better understand the role of IL-10 in Sjogren'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 upregulation 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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M3 - Article
C2 - 10072487
AN - SCOPUS:0033104634
VL - 162
SP - 2488
EP - 2494
JO - Journal of Immunology
JF - Journal of Immunology
SN - 0022-1767
IS - 5
ER -