Short Review
| Rev Diabet Stud,
2009,
6(2):81-84 |
DOI 10.1900/RDS.2009.6.81 |
The Role of the CXCL10/CXCR3 System in Type 1 Diabetes
Akira Shimada1, Yoichi Oikawa1, Yoshifumi Yamada1, Yoshiaki Okubo1, Shosaku Narumi2
1Department of Internal Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan
2Department of Molecular Preventive Medicine, University of Tokyo School of Medicine, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113, Japan
Address correspondence to: Akira Shimada, e-mail: asmd@sc.itc.keio.ac.jp
Manuscript submitted July 27, 2009; resubmitted August 3, 2009; accepted August 7, 2009.
Keywords: type 1 diabetes, GAD, T cell, CD4, CD8, T helper cell, Th1, beta-cell proliferation, NOD, insulitis, CD45RB, IL-10, IL-18, IGRP
Abstract
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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