Beta cell mass in Type 1 diabetes mellitus and islet transplantation

本研究项目将研究β细胞质量和功能丧失的细胞和分子机制：在1型糖尿病（T1 D）的发病机制中;和胰岛移植后。虽然这些过程传统上被认为是纯粹的免疫介导的，但现在清楚的是，β细胞的反应对自身免疫过程的最终结果和对治疗干预的反应至关重要。因此，免疫系统的细胞和可溶性成分之间的复杂相互作用，加上失调的代谢环境的影响，在β细胞中整合。这反过来又激活了β细胞中一系列复杂的转录程序，这些程序共同决定了β细胞的最终功能状态和存活。我们将利用从研究这些过程中获得的知识来推动新的治疗靶点和策略的开发，以提高基于免疫和基于移植的治疗的成功率。

This research program will examine the cellular and molecular mechanisms underlying the loss of Beta cell mass and function: During the pathogenesis of Type 1 Diabetes Mellitus (T1D); and Following islet transplantation. Though these processes have traditionally been considered to be purely immune-mediated, it is now clear that the response of the beta cell is critical to the final outcome of the auto-immune process and response to therapeutic interventions. Thus the complex interactions between the cellular and soluble constituents of the immune system, plus the effects of a deregulated metabolic milieu, are integrated at the beta cell. This in turn activates a series of complex transcriptional programs in the beta cell that together determine the beta cells ultimate functional status and survival. We will use knowledge gained from studying these processes to drive the development of novel therapeutic targets and strategies to improve the success of immune-based and transplantation-based therapies.