Dichotomous roles of co-stimulatory molecules in diabetes mellitus
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Ji-Xin Zhong1, Jie Chen2,3, Xiaoquan Rao2 and Lihua Duan4
1Department of Endocrinology, Central Hospital of Wuhan, Wuhan, Hubei, China 430061
2Cardiovascular Research Institute, School of Medicine, Case Western Reserve University, Cleveland, Ohio, USA 44106
3Basic Medical Department of Medical College, Xiamen University, Xiamen, China 361102
4Department of Rheumatology and Clinical Immunology, The First Affiliated Hospital of Xiamen University, Xiamen, Fujian, China 361003
Lihua Duan, email: firstname.lastname@example.org
Keywords: co-stimulatory molecule; diabetes mellitus; dendritic cells; macrophage; CD28
Received: June 10, 2017 Accepted: November 15, 2017 Published: December 07, 2017
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 cells and T cells have been identified the critical role in the development of diabetes mellitus. Thus, blockage of co-stimulatory dyads interaction between antigen present cells and 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.
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