J Exper Med:科学家揭示模式识别受体NOD2维持肠道粘膜稳态新机制

2013-10-29 中国科学技术大学生科院 中国科学技术大学生科院

近日,中国科学技术大学生命科学学院周荣斌/江维教授研究组和田志刚教授研究组合作,揭示了模式识别受体NOD2维持肠道粘膜稳态的新机制。相关研究成果以“Recognition of gut microbiota by NOD2 is essential for the homeostasis of intestinal intraepithelial lymphocytes”为题在线发表于近日在线发表

近日,中国科学技术大学生命科学学院周荣斌/江维教授研究组和田志刚教授研究组合作,揭示了模式识别受体NOD2维持肠道粘膜稳态的新机制。相关研究成果以“Recognition of gut microbiota by NOD2 is essential for the homeostasis of intestinal intraepithelial lymphocytes”为题在线发表于近日在线发表于《实验医学杂志》(Journal of Experimental Medicine)。

NOD2作为一种胞内的模式识别受体在机体免疫系统抵抗胞内菌感染过程中起重要作用。另外,NOD2也是最早发现的的克罗恩病(Crohn's disease)的易感基因,携带NOD2突变体的人群克罗恩病发病率会显著上升,但是NOD2的多态性影响克罗恩病发生的机制并不清楚。

肠道上皮内淋巴细胞(IEL)作为肠道粘膜免疫的第一道防线,对维持肠道粘膜平衡有着重要作用。本研究发现IEL的数目在Nod2缺陷小鼠中明显降低,而在其它NOD样受体家族蛋白缺陷鼠中没有明显变化。进一步的研究表明NOD2是通过识别肠道共生菌及其活化产生的IL-15维持肠道中IEL的稳定;Nod2缺陷小鼠相对野生型小鼠易发肠炎,如果给Nod2缺陷小鼠转输正常来源的IEL即可缓解小鼠肠炎损伤情况,说明IEL缺失是导致Nod2缺陷小鼠易发肠炎的重要原因。该项研究不仅有助于深入了解IEL的发育分化和稳态维持过程,也提示IEL缺失导致的肠道天然免疫功能低下可能是导致携带NOD2突变体的人群易发克罗恩的潜在原因,从而为该疾病的治疗提供新的思路。本研究得到了国家自然基金委、科技部和中科院的项目资助。

原文出处:

Jiang W, Wang X, Zeng B, Liu L, Tardivel A, Wei H, Han J, Macdonald HR, Tschopp J, Tian Z, Zhou R.Recognition of gut microbiota by NOD2 is essential for the homeostasis of intestinal intraepithelial lymphocytes.J Exp Med. 2013 Oct 21;210(11):2465-76. doi: 10.1084/jem.20122490.

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    2014-05-18 changfy
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    2014-01-27 feather89
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    2014-06-07 hb2008ye
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    2013-10-31 mxj1971616
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    2013-10-31 heli0118