The Role of the CXCL10/CXCR3 System in Type 1 Diabetes

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Abstract
The Review of Diabetic Studies,2009,6,2,81-84.
DOI:10.1900/RDS.2009.6.81
Published:August 2009
Type:Short Review
Authors:
Author(s) affiliations:

Akira Shimada1, Yoichi Oikawa1, Yoshifumi Yamada1, Yoshiaki Okubo1 and 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.

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 betacell 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.

Keywords:Beta-cell proliferation, CD4, CD45RB, CD8, GAD, IGRP, IL-10, IL-18, Insulitis, NOD, T cell, T helper cell, Th1, Type 1 diabetes

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