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Critical Reviews™ in Immunology
Импакт фактор: 1.352 5-летний Импакт фактор: 3.347 SJR: 1.022 SNIP: 0.55 CiteScore™: 2.19

ISSN Печать: 1040-8401
ISSN Онлайн: 2162-6472

Выпуски:
Том 39, 2019 Том 38, 2018 Том 37, 2017 Том 36, 2016 Том 35, 2015 Том 34, 2014 Том 33, 2013 Том 32, 2012 Том 31, 2011 Том 30, 2010 Том 29, 2009 Том 28, 2008 Том 27, 2007 Том 26, 2006 Том 25, 2005 Том 24, 2004 Том 23, 2003 Том 22, 2002 Том 21, 2001 Том 20, 2000 Том 19, 1999 Том 18, 1998 Том 17, 1997 Том 16, 1996 Том 15, 1995 Том 14, 1994

Critical Reviews™ in Immunology

DOI: 10.1615/CritRevImmunol.v20.i2.40
13 pages

Structure of IL-10 and Its Role in Autoimmune Exocrinopathy

Ichiro Saito
Department of Pathology, Tokushima University School of Dentistry, 3-18-15, Kuramotocho, Tokushima 770-8504, Japan

Краткое описание

Cytokines are implicated in the pathogenesis of a variety of autoimmune disorders. Whether the presence of cytokines is primary or secondary and the extent to which these factors may contribute to the development and progression of clinicopathologic alterations in these disorders remain largely unknown but are highly important questions. Our research focuses on evaluating these issues by using a transgenic approach to direct the constitutive expression of cytokines to epithelial cells in the intact exocrine glands of mice. Our recent studies have focused on the potential of the regulatory cytokine IL-10 produced by type 2 T-helper cells to inhibit inflammation and the development of autoimmue diseases. Using targeted introduction of this molecule into the exocrine gland epithelial cells, we found that IL-10 induced apoptosis of glandular tissues destruction and lymphocyte infiltration consisting primarily of Fas-ligand+ CD4+ T cells, as well as in vitro upregulation of FasL expression on T cells. These results suggest that IL-10 is necessary and sufficient for exocrine gland dysfunction in the transgenic mice. This article discusses recent advances in IL-10 and its role in the pathological conditions of autoimmune exocrinopathy.


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