Institute for Medical Microbiology, Immunology and Hygiene, University of Cologne, Germany.
FEBS Lett. 2013 Jul 11;587(14):2137-42. doi: 10.1016/j.febslet.2013.05.037. Epub 2013 May 24.
Innate immune responses induced by the pattern-recognition receptors Nod1 and Nod2 play pivotal roles to combat infection and to instruct adaptive immunity. Here we identify Ankrd17 as a novel binding partner of Nod2 and show that its N-terminal domain mediates Nod2 binding. Knock-down and overexpression analysis revealed that Ankrd17 is functionally involved in Nod2- and Nod1-mediated responses in human myeloid and epithelial cells. In HeLa cells Ankrd17 contributed to pro-inflammatory responses induced by Shigella flexneri, however not to type I interferon responses induced by Sendai virus. In conclusion, this reveals a novel function for Ankrd17 in anti-bacterial innate immune pathways.
模式识别受体 Nod1 和 Nod2 诱导的先天免疫反应对于抵抗感染和指导适应性免疫至关重要。在这里，我们鉴定出 Ankrd17 是 Nod2 的一个新的结合伙伴，并表明其 N 端结构域介导 Nod2 结合。敲低和过表达分析显示，Ankrd17 功能上参与了人髓系和上皮细胞中 Nod2 和 Nod1 介导的反应。在 HeLa 细胞中，Ankrd17 有助于 Shigella flexneri 诱导的促炎反应，但不参与 Sendai 病毒诱导的 I 型干扰素反应。总之，这揭示了 Ankrd17 在抗细菌先天免疫途径中的新功能。
