Immune regulation in type 1 diabetes.
Immune regulation in type 1 diabetes.
复制标题
1 型糖尿病的免疫调节。
DOI：
10.1006/jaut.1996.0033
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发表时间：
1996
影响因子：
12.8
通讯作者：
Fathman,CG
中科院分区：
文献类型：
--
作者：
Shimada,A;Charlton,B;Rohane,P;Taylor-Edwards,C;Fathman,CG
非肥胖糖尿病 (NOD) 小鼠是胰岛素依赖型糖尿病 (IDDM) 的动物模型，显示出人类 IDDM 的许多特征。在 NOD 模型中，胰岛素炎和糖尿病的发病之间存在差异，表明可能存在某种形式的免疫调节来延迟 β 细胞破坏。我们的转移系统使用 NOD-scid/scid (NOD-scid) 小鼠作为供体 NOD 细胞的受体，表明免疫调节细胞存在于 NOD 小鼠的外周，而不是胰岛中。这些调节细胞被认为是记忆性 CD4+ 细胞，在体外激活后显示出 Th2（或 Th0）型细胞因子谱。随着疾病的进展，记忆 CD4+ 细胞的功能似乎从保护性变为致病性。此外，该 CD4+CD45RBlow（记忆）群体的细胞因子谱从 Th2（或 Th0）型反应转变为 Th1 型反应，与高血糖的发生一致。这些数据表明，NOD 疾病从胰岛素炎到明显高血糖的进展受到 CD4+CD45RBlow 免疫“调节”细胞的控制。
The non-obese diabetic (NOD) mouse is an animal model of insulin-dependent diabetes mellitus (IDDM) that shows many of the characteristics of human IDDM. In the NOD model, there exists a discrepancy between the onset of insulitis and diabetes suggesting the potential existence of some form of immune regulation that delays β cell destruction. Our transfer system using NOD-scid/scid (NOD-scid) mice as recipients of donor NOD cells suggested that immune regulatory cells exist in the periphery of NOD mice, not in the islets. These regulatory cells are considered to be memory CD4+cells which show a Th2 (or Th0) type cytokine profile following activationin vitro. The function of the memory CD4+cells seems to change from protective to pathogenic as the disease progresses. Moreover, cytokine profiles of this CD4+CD45RBlow(memory) population shifted from a Th2 (or Th0) to a Th1 type response coincident with the onset of hyperglycaemia. These data suggest that the progression of NOD disease from insulitis to frank hyperglycaemia is under the control of CD4+CD45RBlowimmune ‘regulatory’ cells.