研究人員發(fā)現(xiàn),，即使沒有入侵的微生物或死亡細(xì)胞展示的危險信號，單個壓力應(yīng)答蛋白質(zhì)的表達(dá)也會觸發(fā)免疫細(xì)胞的活躍和大規(guī)模重組,，新成果在線發(fā)表在1月份的《自然—免疫學(xué)》（Nature Immunology）期刊上。
壓力應(yīng)答蛋白質(zhì)通常出現(xiàn)在腫瘤表面，以前的研究懷疑這種壓力應(yīng)答蛋白質(zhì)是否足以激活免疫防御系統(tǒng),。Adrian Hayday和合作者培育了一種小鼠，其壓力應(yīng)答蛋白質(zhì)Rae1可根據(jù)需要開關(guān),。Rae1的引入促發(fā)了皮膚上免疫細(xì)胞的重組,，以及來自血液的受激免疫細(xì)胞的滲透。他們吃驚地發(fā)現(xiàn)，當(dāng)其他地方的免疫細(xì)胞處于抑制狀態(tài)時,，皮膚上的免疫細(xì)胞群卻被激活了,，腫瘤被抑制了。
未來的研究還需要探索蛋白質(zhì)Rae1表達(dá)導(dǎo)致皮膚免疫系統(tǒng)大規(guī)模變化的機(jī)制,，并確定對Rae1表達(dá)的控制能否成為腫瘤治療的方法,。（科學(xué)時報 王丹紅／編譯）
生物谷推薦英文原文：
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: [email protected]
