期刊
JOURNAL OF AUTOIMMUNITY
卷 27, 期 4, 页码 289-296出版社
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.jaut.2006.11.003
关键词
Sjogren's syndrome; salivary glands; autoimmune disease; inflammation; regulatory T cells
类别
资金
- NIAID NIH HHS [R01 AI036938, AI-36938] Funding Source: Medline
- NIAMS NIH HHS [AR-051203, AR047988, AR045222, P50 AR045222, AR049449, R01 AR051203, R01 AR044719, R01 AR049449, R01 AR047988] Funding Source: Medline
- NIDCR NIH HHS [DE-017579] Funding Source: Medline
- NIDDK NIH HHS [K23 DK059850, K23-DK59850, K23 DK059850-05] Funding Source: Medline
IL-2 knockout (KO), IL-2R alpha KO and scurfy mice lack the CD4(+)CD25(+) regulatory T (Treg) cells and develop severe inflammation in multiple organs, although organs affected vary among these strains. We asked if salivary and lacrimal glands, the main organs affected in Sjogren's syndrome, are targeted in these strains. Severe lymphocyte and neutrophil infiltration in the salivary and lacrimal glands and a decrease in salivary secretory function were observed in IL-2 KO and IL-2Ra KO mice, but not in scurfy mice. Interestingly, transfer of lymph node cells from scurfy mice to RAG-I KO recipients rapidly and effectively induced inflammation and loss of function in the salivary glands. Furthermore, we observed that daily LPS feeding in scurfy mice also induced inflammation in the salivary glands. Our study demonstrates several novel models for Sjogren's syndrome, including an adoptive transfer model that shows that scurfy mice have dormant salivary gland-specific autoreactive lymphocytes that can be activated by certain environmental factors, such as those present in RAG-1 KO mice. (c) 2006 Elsevier Ltd. All rights reserved.
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