研究人员发现，即使没有入侵的微生物或死亡细胞展示的危险信号，单个压力应答蛋白质的表达也会触发免疫细胞的活跃和大规模重组，新成果在线发表在1月份的《自然—免疫学》（Nature Immunology）期刊上。
压力应答蛋白质通常出现在肿瘤表面，以前的研究怀疑这种压力应答蛋白质是否足以激活免疫防御系统。Adrian Hayday和合作者培育了一种小鼠，其压力应答蛋白质Rae1可根据需要开关。Rae1的引入促发了皮肤上免疫细胞的重组，以及来自血液的受激免疫细胞的渗透。他们吃惊地发现，当其他地方的免疫细胞处于抑制状态时，皮肤上的免疫细胞群却被激活了，肿瘤被抑制了。
未来的研究还需要探索蛋白质Rae1表达导致皮肤免疫系统大规模变化的机制，并确定对Rae1表达的控制能否成为肿瘤治疗的方法。（科学时报 王丹红／编译）
生物谷推荐英文原文：
Nature Immunology
Published online: 6 January 2008 | doi:10.1038/ni1556
Acute upregulation of an NKG2D ligand promotes rapid reorganization of a local immune compartment with pleiotropic effects on carcinogenesis
Jessica Strid1, Scott J Roberts2, Renata B Filler2, Julia M Lewis2, Bernice Y Kwong2, William Schpero2, Daniel H Kaplan3, Adrian C Hayday1,4 & Michael Girardi2,4
Abstract
The self-encoded ligands MICA (human) and Rae-1 (mouse) for the cytotoxic lymphocyte activating receptor NKG2D are highly expressed in carcinomas and inflammatory lesions and have been linked to immunosurveillance and graft rejection. However, whether NKG2D ligands have an intrinsic ability to acutely regulate tissue-associated immune compartments is not known. Here we show that epidermis-specific upregulation of Rae-1 induced rapid, coincident and reversible changes in the organization of tissue-resident V5V1 TCR+ intraepithelial T cells and Langerhans cells, swiftly followed by epithelial infiltration by unconventional T cells. Whereas local V5V1+ T cells limited carcinogenesis, Langerhans cells unexpectedly promoted it. These results provide unique insight into the early phases of tissue immunosurveillance and indicate that acute changes in NKG2D ligands may alone initiate a rapid, multifaceted immunosurveillance response in vivo.
Peter Gorer Department of Immunobiology, King's College London School of Medicine at Guy's Hospital, London SE1 9RT, UK.
Department of Dermatology and Skin Diseases Research Center, Yale University School of Medicine, New Haven, Connecticut 06511, USA.
Department of Dermatology and Center for Immunology, University of Minnesota, Minneapolis, Minnesota 55455, USA.
These authors contributed equally to this work.
Correspondence to: Adrian C Hayday1,4 e-mail: adrian.hayday@kcl.ac.uk
