據(jù)新華社北京7月15日電,，一個國際研究小組14日報告說,，他們發(fā)現(xiàn)了一種淋巴細胞的數(shù)量調(diào)節(jié)機制。這種淋巴細胞被稱為調(diào)節(jié)性T細胞,，具有抑制免疫反應(yīng)的功能,。這項發(fā)現(xiàn)有助于開發(fā)免疫功能紊亂的新療法。
由歐盟,、比利時政府,、澳大利亞國家健康和醫(yī)療研究委員會等機構(gòu)資助的一個國際研究小組報告說，他們發(fā)現(xiàn)盡管人體內(nèi)會不斷生成新的調(diào)節(jié)性T細胞,，但它們的總數(shù)量由細胞凋亡過程控制,。
細胞凋亡是指為維持內(nèi)環(huán)境穩(wěn)定，由基因控制的細胞程序性死亡,。研究領(lǐng)導(dǎo)者之一,、澳大利亞墨爾本沃爾特·伊麗莎研究所博士丹尼爾·格雷解釋說，他們發(fā)現(xiàn)一種名為Bcl－2的基因?qū)φ{(diào)節(jié)性T細胞數(shù)量起到?jīng)Q定性作用,。具體來說,，調(diào)節(jié)性T細胞的數(shù)量由Bcl－2家族蛋白質(zhì)中兩種功能相反的蛋白質(zhì)決定，它們分別被稱為Mcl－1蛋白質(zhì)和Bim蛋白質(zhì),。其中,，Mcl－1蛋白質(zhì)能幫助調(diào)節(jié)性T細胞存活，而Bim蛋白質(zhì)則引發(fā)調(diào)節(jié)性T細胞死亡,。如果人體內(nèi)Mcl－1蛋白質(zhì)的活性被抑制,，那么調(diào)節(jié)性T細胞數(shù)量就會下降，從而引發(fā)自體免疫疾??；相反如果人體內(nèi)Bim蛋白質(zhì)活性被抑制，調(diào)節(jié)性T細胞數(shù)量會不正常地升高,。
研究人員表示,，這項發(fā)現(xiàn)為控制某些患者體內(nèi)調(diào)節(jié)性T細胞數(shù)量打開一條新路。相關(guān)論文已經(jīng)發(fā)表在最新一期英國《自然－免疫學(xué)》雜志上,。（生物谷 Bioon.com）
生物谷推薦的英文摘要
Nature Immunology doi:10.1038/ni.2649
Antiapoptotic Mcl-1 is critical for the survival and niche-filling capacity of Foxp3+ regulatory T cells
Wim Pierson, Bénédicte Cauwe, Antonia Policheni, Susan M Schlenner, Dean Franckaert, Julien Berges, Stephanie Humblet-Baron, Susann Schönefeldt, Marco J Herold, David Hildeman, Andreas Strasser, Philippe Bouillet, Li-Fan Lu, Patrick Matthys, Antonio A Freitas, Rita J Luther, Casey T Weaver, James Dooley, Daniel H D Gray & Adrian Liston
Foxp3+ regulatory T (Treg) cells are a crucial immunosuppressive population of CD4+ T cells, yet the homeostatic processes and survival programs that maintain the Treg cell pool are poorly understood. Here we report that peripheral Treg cells markedly alter their proliferative and apoptotic rates to rapidly restore numerical deficit through an interleukin 2–dependent and costimulation-dependent process. By contrast, excess Treg cells are removed by attrition, dependent on the Bim-initiated Bak- and Bax-dependent intrinsic apoptotic pathway. The antiapoptotic proteins Bcl-xL and Bcl-2 were dispensable for survival of Treg cells, whereas Mcl-1 was critical for survival of Treg cells, and the loss of this antiapoptotic protein caused fatal autoimmunity. Together, these data define the active processes by which Treg cells maintain homeostasis via critical survival pathways.
