T Cell-Mediated Beta Cell Destruction: Autoimmunity and Alloimmunity in the Context of Type 1 Diabetes.
T Cell-Mediated Beta Cell Destruction: Autoimmunity and Alloimmunity in the Context of Type 1 Diabetes.
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DOI：
10.3389/fendo.2017.00343
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发表时间：
2017
影响因子：
5.2
通讯作者：
Fife BT
中科院分区：
文献类型：
--
作者：
Burrack AL;Martinov T;Fife BT
1型糖尿病（T1D）是由免疫系统的T细胞破坏胰腺β细胞引起的。尽管胰岛素类似物和连续血糖水平监测有所改善，但T1D仍无法治愈，有些人会出现危及生命的并发症。胰腺和胰岛移植一直是有吸引力的治疗方法，然而，含有胰岛素产生细胞的移植物易受复发性自身免疫和常规同种异体移植物排斥的影响。目前的免疫抑制治疗抑制免疫系统，但并非没有并发症。理想情况下，成功的方法应该只针对破坏性的免疫细胞，而让剩余的免疫系统完整地对抗外来病原体。这篇综述讨论了自身免疫性糖尿病的过程，糖尿病并发症，保证移植，同种异体免疫。首先，我们描述了目前对β细胞自身免疫破坏的理解，包括CD4和CD8 T细胞的作用以及抗原特异性耐受诱导的几种可能性。其次，我们概述了糖尿病并发症需要β细胞替代。第三，我们讨论了移植识别，β细胞替代的潜在来源，以及正在开发的促进耐受性的疗法。我们假设，更好地了解疾病发病过程中的自身反应性T细胞靶点和移植破坏后的同种异体免疫，可以增强重建对β细胞耐受性的尝试。
Type 1 diabetes (T1D) results from destruction of pancreatic beta cells by T cells of the immune system. Despite improvements in insulin analogs and continuous blood glucose level monitoring, there is no cure for T1D, and some individuals develop life-threatening complications. Pancreas and islet transplantation have been attractive therapeutic approaches; however, transplants containing insulin-producing cells are vulnerable to both recurrent autoimmunity and conventional allograft rejection. Current immune suppression treatments subdue the immune system, but not without complications. Ideally a successful approach would target only the destructive immune cells and leave the remaining immune system intact to fight foreign pathogens. This review discusses the autoimmune diabetes disease process, diabetic complications that warrant a transplant, and alloimmunity. First, we describe the current understanding of autoimmune destruction of beta cells including the roles of CD4 and CD8 T cells and several possibilities for antigen-specific tolerance induction. Second, we outline diabetic complications necessitating beta cell replacement. Third, we discuss transplant recognition, potential sources for beta cell replacement, and tolerance-promoting therapies under development. We hypothesize that a better understanding of autoreactive T cell targets during disease pathogenesis and alloimmunity following transplant destruction could enhance attempts to re-establish tolerance to beta cells.
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