调节性不变自然杀伤T细胞在预防1型糖尿病中的作用。

Role of regulatory invariant CD1d-restricted natural killer T-cells in protection against type 1 diabetes.

作者信息

Hussain Shabbir, Wagner Melany, Ly Dalam, Delovitch Terry L

机构信息

Autoimmunity/Diabetes Group, Robarts Research Institute, 1400 Western Road, London, Ontario N6G 2V4, Canada.

出版信息

Immunol Res. 2005;31(3):177-88. doi: 10.1385/IR:31:3:177.

DOI:10.1385/IR:31:3:177

PMID:15888910

Abstract

Invariant CD1d-restricted natural killer T (iNKT) cells function during innate and adaptive immune responses. A functional and numerical deficiency of iNKT cells is well documented in both nonobese diabetic (NOD) mice and humans with autoimmune type 1 diabetes (T1D). Restoring the numerical and/or functional deficiency of iNKT cells in NOD mice by either treatment with alpha-galactosylceramide, transgenic induction of Valpha14-Jalpha18 expression, or transgenic expression of CD1d in NOD islets under the control of the human insulin promoter confers protection from T1D in these mice. Recently, considerable progress has been made in understanding the developmental and functional activities of iNKT cells. In this review, we discuss the role of iNKT cell deficiency and defective development in the onset of T1D in NOD mice and the different protective mechanisms known to restore these defects.

摘要

不变自然杀伤T（iNKT）细胞在先天性和适应性免疫反应中发挥作用。在非肥胖糖尿病（NOD）小鼠和患有自身免疫性1型糖尿病（T1D）的人类中，iNKT细胞的功能和数量缺陷均有充分记录。通过用α-半乳糖神经酰胺治疗、转基因诱导Vα14-Jα18表达或在人胰岛素启动子控制下在NOD胰岛中进行CD1d的转基因表达来恢复NOD小鼠中iNKT细胞的数量和/或功能缺陷，可使这些小鼠免受T1D的侵害。最近，在了解iNKT细胞的发育和功能活动方面取得了相当大的进展。在这篇综述中，我们讨论了iNKT细胞缺陷和发育缺陷在NOD小鼠T1D发病中的作用，以及已知的恢复这些缺陷的不同保护机制。