Advances in our understanding of the pathophysiology of Type 1 diabetes: lessons from the NOD mouse

被引：45
作者：
Jayasimhan, Abhirup [1 ]
Mansour, Kristy P. [1 ]
Slattery, Robyn M. [1 ]
机构：
[1] Monash Univ, Alfred Hosp Med Res & Educ Precinct AMREP, Dept Immunol, Melbourne, Vic 3004, Australia
来源：
CLINICAL SCIENCE | 2014年 / 126卷 / 1-2期
关键词：
autoimmunity; immunopathogenesis; insulitis; non-obese diabetic mouse (NOD mouse); Type 1 diabetes (T10); PANCREATIC LYMPH-NODES; DIABETOGENIC T-CELLS; INTERCELLULAR-ADHESION MOLECULE-1; CLASS-II MOLECULE; MHC CLASS-I; BETA-CELLS; B-CELLS; RECENT-ONSET; DENDRITIC CELLS; CYTOKINE PRODUCTION;
D O I：
10.1042/CS20120627
中图分类号：
R-3 [医学研究方法]; R3 [基础医学];
学科分类号：
1001 ;
摘要：
T1D (Type 1 diabetes) is an autoimmune disease caused by the immune-mediated destruction of pancreatic beta-cells. Studies in T1D patients have been limited by the availability of pancreatic samples, a protracted pre-diabetic phase and limitations in markers that reflect beta-cell mass and function. The NOD (non-obese diabetic) mouse is currently the best available animal model of T1D, since it develops disease spontaneously and shares many genetic and immunopathogenic features with human T1D. Consequently, the NOD mouse has been extensively studied and has made a tremendous contribution to our understanding of human T1D. The present review summarizes the key lessons from NOD mouse studies concerning the genetic susceptibility, aetiology and immunopathogenic mechanisms that contribute to autoimmune destruction of beta-cells. Finally, we summarize the potential and limitations of immunotherapeutic strategies, successful in NOD mice, now being trialled in T1D patients and individuals at risk of developing T1D.
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页码：1 / 18
页数：18
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