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The Role of the CXCL10/CXCR3 System in Type 1 Diabetes
Author(s) -
Akira Shimada,
Yoichi Oikawa,
Yoshifumi Yamada,
Yoshiaki Okubo,
Shosaku Narumi
Publication year - 2009
Publication title -
the review of diabetic studies
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.701
H-Index - 41
eISSN - 1614-0575
pISSN - 1613-6071
DOI - 10.1900/rds.2009.6.81
Subject(s) - cxcr3 , immune system , immunology , cxcl10 , diabetes mellitus , type 2 diabetes , medicine , beta cell , type 1 diabetes , disease , t cell , ccl18 , chemokine , chemokine receptor , endocrinology , islet
Despite intervention with insulin, type 1 diabetes gradually deteriorates the patients' quality of life. The disease is characterized by an immune-mediated destruction of pancreatic beta-cells. Its etiology, however, remains controversial. Some studies argue that glutamic acid decarboxylase (GAD) antigen and GAD-reactive T cells are critical players in the development of diabetes by affecting the Th cell balance. A T-helper 1 (Th1)-dominant immune response is considered to be important in beta-cell failure in both human and animal models of type 1 diabetes. The Th1-type chemokine, CXCL10, and its receptor, CXCR3, are involved not only in the immune response, but also in the suppression of beta-cell proliferation. Thus, understanding the CXCL10/CXCR3 system may be important for finding a cure. In this short review, we discuss the role of the CXCL10/CXCR3 system in type 1 diabetes and propose relevant treatment options.

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