The role of the CXCL10/CXCR3 system in type 1 diabetes.

Department of Internal Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.
The Review of Diabetic Studies 01/2009; 6(2):81-4. DOI: 10.1900/RDS.2009.6.81
Source: PubMed

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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