McLaughlin Rene J, Spindler Matthew P, van Lummel Menno, Roep Bart O
Department of Immunohematology and Blood Transfusion, Leiden University Medical Center, E3-Q, PO Box 9600, 2300 RC, Leiden, The Netherlands.
Department of Diabetes Immunology, Diabetes & Metabolism Research Institute, Beckman Research Institute of City of Hope, Duarte, CA, 91010, USA.
Curr Diab Rep. 2016 Jul;16(7):63. doi: 10.1007/s11892-016-0752-4.
Autoreactive T cells specific for islet autoantigens develop in type 1 diabetes (T1D) by escaping central as well as peripheral tolerance. The current paradigm for development of islet autoimmunity is just beginning to include the contribution of posttranslationally modified (PTM) islet autoantigens, for which the immune system may be ignorant rather than tolerant. As a result, PTM is the latest promising lead in the quest to understand how the break in peripheral tolerance occurs in T1D. However, it is not completely clear how, where, or when these modifications take place. Currently, only a few PTM antigens have been well-thought-out or identified in T1D, and methods for identifying and characterizing new PTM antigens are rapidly improving. This review will address both reported and potential new sources of modified islet autoantigens and discuss how islet neo-autoantigen generation may contribute to the development and progression of T1D.
1型糖尿病（T1D）中，针对胰岛自身抗原的自身反应性T细胞通过逃避中枢和外周耐受而产生。目前关于胰岛自身免疫发展的范例才刚刚开始纳入翻译后修饰（PTM）的胰岛自身抗原的作用，免疫系统对这些抗原可能处于忽视而非耐受状态。因此，PTM是探寻T1D中外周耐受如何被打破的最新且有前景的线索。然而，目前尚不完全清楚这些修饰是如何、在何处以及何时发生的。目前，在T1D中仅有少数PTM抗原得到了充分的研究或鉴定，并且鉴定和表征新的PTM抗原的方法正在迅速改进。本综述将探讨已报道的和潜在的修饰胰岛自身抗原的新来源，并讨论胰岛新自身抗原的产生如何可能促进T1D的发生和发展。
Zotero 插件