科学家们鉴别出一种新蛋白质，这种蛋白质能探测和控制那些逃离宿主防御系统的细菌。他们在日前在线出版的《自然―免疫学》期刊上报道，这种蛋白质与高度致病性细菌的去除有关。
尽管有害的细菌一般均会隐蔽在人体宿主细胞中的一个隔间中，如导致伤寒和肠胃炎的沙门氏菌，但这些细菌也会偶尔逃离这个隔间并侵入宿主细胞。因尚未查明的原因，这些逃离的细菌通常会披上宿主蛋白质泛素。
Felix Randow和同事发现，宿主蛋白质NDP52与这些披上泛素外衣的细菌捆绑在一起，应要求消灭入侵的细菌。通过征集其他的宿主防御蛋白质，NDP52好像促进了细菌的自我吞噬。当然，还需要做进一步的工作以精确确定，究竟有多少致病性细胞受NDP52控制。
英文原文原始出处及摘要：
Nature Immunology 10, 1215 - 1221 (2009) 11 October 2009 | doi:10.1038/ni.1800
The TBK1 adaptor and autophagy receptor NDP52 restricts the proliferation of ubiquitin-coated bacteria
Teresa L M Thurston1,3, Grigory Ryzhakov1,2,3, Stuart Bloor1,3, Natalia von Muhlinen1 " Felix Randow1
Cell-autonomous innate immune responses against bacteria attempting to colonize the cytosol of mammalian cells are incompletely understood. Polyubiquitylated proteins can accumulate on the surface of such bacteria, and bacterial growth is restricted by Tank-binding kinase (TBK1). Here we show that NDP52, not previously known to contribute to innate immunity, recognizes ubiquitin-coated Salmonella enterica in human cells and, by binding the adaptor proteins Nap1 and Sintbad, recruits TBK1. Knockdown of NDP52 and TBK1 facilitated bacterial proliferation and increased the number of cells containing ubiquitin-coated salmonella. NDP52 also recruited LC3, an autophagosomal marker, and knockdown of NDP52 impaired autophagy of salmonella. We conclude that human cells utilize the ubiquitin system and NDP52 to activate autophagy against bacteria attempting to colonize their cytosol.
1 Medical Research Council Laboratory of Molecular Biology, Division of Protein and Nucleic Acid Chemistry, Cambridge, UK.
2 Present address: Kennedy Institute of Rheumatology, Imperial College London, London, UK.
3 These authors contributed equally to this work.
