NKG2D 在炎症和自身免疫性疾病中的选择性作用。
A selective role of NKG2D in inflammatory and autoimmune diseases.
机构信息
Department of Molecular and Cell Biology, and Cancer Research Laboratory, 489 Life Sciences, Addition, University of California at Berkeley, Berkeley, CA 94720, USA.
Department of Life Science, Imperial College London, Imperial College Road, SW7 2AZ, London.
出版信息
Clin Immunol. 2013 Dec;149(3):432-9. doi: 10.1016/j.clim.2013.09.003. Epub 2013 Sep 14.
The NKG2D activating receptor has been implicated in numerous autoimmune diseases. We tested the role of NKG2D in models of autoimmunity and inflammation using NKG2D knockout mice and antibody blockade experiments. The severity of experimental autoimmune encephalitis (EAE) was decreased in NKG2D-deficient mice when the disease was induced with a limiting antigen dose, but unchanged with an optimal antigen dose. Surprisingly, however, NKG2D deficiency had no detectable effect in several other models, including two models of type 1 diabetes, and a model of intestinal inflammation induced by poly(I:C). NKG2D antibody blockade in normal mice also failed to inhibit disease in the NOD diabetes model or the intestinal inflammation model. Published evidence using NKG2D knockout mice demonstrated a role for NKG2D in mouse models of atherosclerosis and liver inflammation, as well as in chronic obstructive pulmonary disease. Therefore, our results suggest that NKG2D plays selective roles in inflammatory diseases.
NKG2D 激活受体与许多自身免疫性疾病有关。我们使用 NKG2D 敲除小鼠和抗体阻断实验来测试 NKG2D 在自身免疫和炎症模型中的作用。在使用限制抗原剂量诱导实验性自身免疫性脑脊髓炎 (EAE) 时，NKG2D 缺陷小鼠的疾病严重程度降低，但在使用最佳抗原剂量时无变化。然而，令人惊讶的是，NKG2D 缺陷在其他几种模型中没有明显作用，包括两种 1 型糖尿病模型和聚（I:C）诱导的肠道炎症模型。在正常小鼠中使用 NKG2D 抗体阻断也未能抑制 NOD 糖尿病模型或肠道炎症模型中的疾病。使用 NKG2D 敲除小鼠的已发表证据表明 NKG2D 在动脉粥样硬化和肝脏炎症以及慢性阻塞性肺疾病的小鼠模型中起作用。因此，我们的结果表明 NKG2D 在炎症性疾病中发挥选择性作用。
Zotero 插件