NKG2D blockade prevents autoimmune diabetes in NOD mice
NKG2D blockade prevents autoimmune diabetes in NOD mice
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DOI：
10.1016/j.immuni.2004.05.008
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发表时间：
2004-06-01
期刊：
影响因子：
32.4
通讯作者：
Lanier, LL
中科院分区：
文献类型：
--
作者：
Ogasawara, K;Hamerman, JA;Lanier, LL
NKG 2D是CD 8（+）T细胞和NK细胞上的一种活化受体，与抗肿瘤和微生物病原体的免疫有关。我们发现RAE-1存在于NOD小鼠的糖尿病前期胰岛中，浸润胰腺的自身反应性CD 8（+）T细胞表达NKG 2D。在糖尿病前期阶段使用非消耗性抗NKG 2D单克隆抗体（mAb）治疗，通过损害自身反应性CD 8（+）T细胞的扩增和功能，完全预防了疾病。这些发现表明NKG 2D对疾病进展至关重要，并提出了自身免疫性I型糖尿病的新治疗靶点。
NKG2D is an activating receptor on CD8(+) T cells and NK cells that has been implicated in immunity against tumors and microbial pathogens. Here we show that RAE-1 is present in prediabetic pancreas islets of NOD mice and that autoreactive CD8(+) T cells infiltrating the pancreas express NKG2D. Treatment with a nondepleting anti-NKG2D monoclonal antibody (mAb) during the prediabetic stage completely prevented disease by impairing the expansion and function of autoreactive CD8(+) T cells. These findings demonstrate that NKG2D is essential for disease progression and suggest a new therapeutic target for autoimmune type I diabetes.