The non obese diabetic (NOD) mouse: a unique model for understanding the interaction between genetics and T cell responses.
The non obese diabetic (NOD) mouse: a unique model for understanding the interaction between genetics and T cell responses.
复制标题
非肥胖糖尿病 (NOD) 小鼠：了解遗传学和 T 细胞反应之间相互作用的独特模型。
DOI：
10.1023/a:1025104429334
复制
发表时间：
2003
影响因子：
8.2
通讯作者：
Ridgway,WilliamM
中科院分区：
文献类型：
--
作者：
Ridgway,WilliamM
The first demonstration that NOD diabetes was autoimmune in etiology was that splenic cells from diabetic mice transferred diabetes to young irradiated NOD recipients [1]. Purified CD4+ cells also transferred disease, implicating the CD4+ subset in pathogenesis [2, 3]. As few as 500 CD4high memory/activated Th1 (IFN-γ producing) cells transferred disease into NOD-scid mice, demonstrating that activated, cytokine effector Th1-biased cells were specifically pathogenic in very small numbers [4]. The role of CD4+ T cells was further demonstrated by many studies showing that anti-T cell and specifically anti-CD4 directed therapies could prevent diabetes in NOD mice [5]. Moreover, anti-CD3 treatment was one of the few therapies demonstrated to reverse established autoimmune murine diabetes [6]. Finally, the NOD MHC Class II molecule, IA g7, was unique in structure and shared a specific amino acid substitution in common with the disease associated human MHC Class II allele [7]. The NOD MHC Class II region was one of the strongest linkages to autoimmunity, and class II homozygosity was essential for diabetes [8], providing further evidence supporting a role for CD4+ T cells in pathogenesis.
