Auto- and alloreactive T cells are major culprits that damage β-cells in type 1 diabetes(T1D) and islet transplantation. Current immunosuppressive drugs can alleviate immune-mediated attacks on islets. T cell co-stimulation blockade has shown great promise in autoimmunity and transplantation as it solely targets activated T cells, and therefore avoids toxicity of current immunosuppressive drugs. An attractive approach is offered by the newly-identified negative T cell cosignaling molecule B7-H4 which is expressed in normal human islets, and its expression co-localizes with insulin. A concomitant decrease in B7-H4/insulin colocalization is observed in human type 1 diabetic islets. B7-H4 may play protective roles in the pancreatic islets, preserving their function and survival. In this review we outline the protective effect of B7-H4 in the contexts of T1 D, islet cell transplantation, and potentially type 2 diabetes. Current evidence offers encouraging data regarding the role of B7-H4 in reversal of autoimmune diabetes and donor-specific islet allograft tolerance. Additionally, unique expression of B7-H4 may serve as a potential biomarker for the development of T1 D. Futurestudies should continue to focus on the islet-specific effects of B7-H4 with emphasis on mechanistic pathways in order to promote B7-H4 as a potential therapy and cure for T1 D.
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机译:Fucoidan ameliorates pancreatic 尾鈥恈ell death and impaired insulin synthesis in streptozotocin鈥恡reated 尾 cells and mice via a Sirt鈥?鈥恉ependent manner
机译:Fucoidan ameliorates pancreatic 尾鈥恈ell death and impaired insulin synthesis in streptozotocin鈥恡reated 尾 cells and mice via a Sirt鈥?鈥恉ependent manner
机译:Real-time Simultaneous Measurement of Pancreatic β Cell Electrophysiology and Fluorescent Bioimaging Based on High-resolution Thin-film Transistor Microelectrode Arrays
机译:Retraction Notice: Jinshui He Xu Zhang Chaowei Lian Jinzhi Wu Yanling Fang Xiaoling Ye. Exendin-4 prevented pancreatic beta cells from apoptosis in (Type I) diabetic mouse via keap1-Nrf2 signaling