Shimada Akira, Oikawa Yoichi, Yamada Yoshifumi, Okubo Yoshiaki, Narumi Shosaku
Department of Internal Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.
Rev Diabet Stud. 2009;6(2):81-4. doi: 10.1900/RDS.2009.6.81. Epub 2009 Aug 10.
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.
尽管使用胰岛素进行干预，但1型糖尿病仍会逐渐降低患者的生活质量。该疾病的特征是胰腺β细胞受到免疫介导的破坏。然而，其病因仍存在争议。一些研究认为，谷氨酸脱羧酶（GAD）抗原和GAD反应性T细胞通过影响Th细胞平衡，在糖尿病的发展中起着关键作用。在1型糖尿病的人类和动物模型中，以辅助性T细胞1（Th1）为主导的免疫反应被认为在β细胞功能衰竭中很重要。Th1型趋化因子CXCL10及其受体CXCR3不仅参与免疫反应，还参与抑制β细胞增殖。因此，了解CXCL10/CXCR3系统可能对找到治愈方法很重要。在这篇简短的综述中，我们讨论了CXCL10/CXCR3系统在1型糖尿病中的作用，并提出了相关的治疗选择。
