The Role of the CXCL10/CXCR3 System in Type 1 Diabetes
Akira Shimada , Yoichi Oikawa , Yoshifumi Yamada, Yoshiaki OkuboDepartment of Internal Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.
Shosaku NarumiDepartment of Molecular Preventive Medicine, University of Tokyo School of Medicine, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113, Japan.
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.
Keywordstype 1 diabetes · GAD · T cell · CD4 · CD8 · T helper cell · Th1 · beta-cell proliferation · NOD · insulitis · CD45RB · IL-10 · IL-18 · IGRP,.
Rev Diabet Stud