Clinical application of NKT cell biology in type I (autoimmune) diabetes mellitus

被引：13

作者：

Fletcher, Marie T. ^{[2
]}

Baxter, Alan G. ^{[1
]}

机构：

[1] James Cook Univ, Comparat Genom Ctr, Townsville, Qld 4811, Australia

[2] Univ Melbourne, Dept Microbiol & Immunol, Parkville, Vic 3052, Australia

来源：

IMMUNOLOGY AND CELL BIOLOGY | 2009年 / 87卷 / 04期

基金：

英国医学研究理事会;

关键词：

immunoregulation; autoimmunity; mouse models; tolerance; KILLER T-CELLS; MAJOR HISTOCOMPATIBILITY COMPLEX; CENTRAL-NERVOUS-SYSTEM; NOD MICE; DENDRITIC CELLS; CUTTING EDGE; SUBCONGENIC ANALYSIS; CYTOKINE PRODUCTION; PERIPHERAL-BLOOD; CD1D EXPRESSION;

D O I：

10.1038/icb.2009.5

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Type 1 natural killer T (NKT) cells are a population of CD1d-restricted, regulatory T cells that exhibit various NK cell characteristics and rapidly produce cytokines on stimulation with glycolipid antigen. In type I diabetes (TID), NKT cells are thought to have a tolerogenic function, evidenced by NKT cell numerical and functional deficiencies in the nonobese diabetic ( NOD) mouse, which when corrected, can ameliorate disease. The mechanisms by which NKT cells can mediate their immunosuppressive effects in NOD mice are still poorly understood, which makes successful clinical translation of NKT-cell-based therapies challenging. However, new insights into the genetic control of NKT cell deficiencies have provided some understanding of the genes that may control NKT cell number and function, potentially offering a new avenue for assessing TID risk in humans. Here, we review the mechanisms by which NKT cells are thought to prevent TID, discuss the evidence for involvement of NKT cells in the regulation of human TID and examine the genetic control of NKT cell number and function. A greater understanding of these areas will increase the chances of successful clinical manipulation of NKT cells to prevent or treat TID. Immunology and Cell Biology ( 2009) 87, 315-323; doi:10.1038/icb.2009.5; published online 17 February 2009

引用

页码：315 / 323

页数：9

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