Dichotomous roles of co-stimulatory molecules in diabetes mellitus

// Ji-Xin Zhong 1 , Jie Chen 2, 3 , Xiaoquan Rao 2 and Lihua Duan 4 1 Department of Endocrinology, Central Hospital of Wuhan, Wuhan, Hubei, China 430061 2 Cardiovascular Research Institute, School of Medicine, Case Western Reserve University, Cleveland, Ohio, USA 44106 3 Basic Medical Department of Medical College, Xiamen University, Xiamen, China 361102 4 Department of Rheumatology and Clinical Immunology, The First Affiliated Hospital of Xiamen University, Xiamen, Fujian, China 361003 Correspondence to: Lihua Duan, email: lh-duan@163.com Keywords: co-stimulatory molecule; diabetes mellitus; dendritic cells; macrophage; CD28Received: June 10, 2017 Accepted: November 15, 2017 Published: December 07, 2017 ABSTRACT Numerous studies have established the importance of immune dysfunction in the development of diabetes mellitus, including typ1 and typ2 diabetes, and it is worth noting that T cell activation acts a key role in the pathogenesis of loss of β cell mass, adipose inflammation and insulin resistance. Regarding as an important checkpoint in the process of T cell activation, co-stimulatory molecules interaction between antigen present cellsand T cells have been identified the critical role in the development of diabetes mellitus. Thus, blockage of co-stimulatory dyads interaction between antigen present cellsand T cells was supposed to a potential of therapeutic strategies. However, studies also showed that inhibition or deletion of some co-stimulatory molecules do not always reduce the development of diabetes, and even exacerbate the disease activity. Here, in this context, we highlight the dichotomous role of co-stimulatory molecules interaction in the pathogenesis of diabetes.