日本京都大學(xué)再生醫(yī)學(xué)科學(xué)研究所的一個(gè)研究小組經(jīng)研究發(fā)現(xiàn),，對(duì)人體免疫功能有調(diào)節(jié)作用的T細(xì)胞（胸腺依賴淋巴細(xì)胞）按活力大小可分為“活性型”與“非活性型”兩種,。該成果發(fā)表在22日的美國(guó)免疫學(xué)雜志《免疫》電子版上,。
T細(xì)胞是哺乳動(dòng)物體內(nèi)抑制免疫反應(yīng)的淋巴細(xì)胞群,。據(jù)稱,，研究人員在人體T細(xì)胞表面分子上使用了一種帶標(biāo)志的抗體,，來(lái)調(diào)查T(mén)細(xì)胞的反應(yīng),。結(jié)果發(fā)現(xiàn)T細(xì)胞對(duì)抗體的反應(yīng)分為兩種,，一種離開(kāi)了抗體,，一種則與抗體緊密結(jié)合在一起。研究人員據(jù)此將其分別命名為“活性型”和“非活性型”,。
研究發(fā)現(xiàn),，活性型T細(xì)胞對(duì)免疫反應(yīng)的抑制力很強(qiáng)，而非活性型的抑制力則很小,，不過(guò)受到相應(yīng)刺激的話,，非活性型可以轉(zhuǎn)化成活性型。對(duì)于人類(lèi),，胎兒的血液中非活性型T細(xì)胞比較多,，上了年紀(jì)的老人體內(nèi)則是活性型T細(xì)胞比較多。
研究人員稱,，自身免疫疾病和臟器移植中排斥反應(yīng)的輕重與這兩種T細(xì)胞的比例有直接關(guān)系,，如果活性型T細(xì)胞減少，就容易患病或出現(xiàn)排斥反應(yīng),。而如果能夠控制這兩種T細(xì)胞的比例,，找到抑制排斥反應(yīng)的方法，就有可能開(kāi)發(fā)出治療自身免疫障礙和過(guò)敏性疾病，以及抑制臟器移植過(guò)程中排斥反應(yīng)的藥品,。（生物谷Bioon.com）
生物谷推薦原始出處：
Immunity, 21 May 2009 doi:10.1016/j.immuni.2009.03.019
Functional Delineation and Differentiation Dynamics of Human CD4+ T Cells Expressing the FoxP3 Transcription Factor
Makoto Miyara1,10,Yumiko Yoshioka1,9,Akihiko Kitoh1,9,Tomoko Shima1,9,Kajsa Wing1,Akira Niwa2,Christophe Parizot3,Cécile Taflin3,Toshio Heike2,Dominique Valeyre4,Alexis Mathian3,Tatsutoshi Nakahata2,Tomoyuki Yamaguchi1,Takashi Nomura1,Masahiro Ono1,Zahir Amoura5,6,Guy Gorochov3,6andShimon Sakaguchi1,7,8,,
1 Department of Experimental Pathology, Institute for Frontier Medical Sciences, Kyoto University, Kyoto 606-8507, Japan
2 Department of Pediatrics, Graduate School of Medicine, Kyoto University, Kyoto 606-8507, Japan
3 Institut National de la Santé et de la Recherche Médicale (INSERM) UMR-S 945, Laboratoire AP-HP d'immunologie cellulaire et tissulaire, H?pital Pitié-Salpêtrière, 75013 Paris, France
4 Pneumology Department, AP-HP H?pital Avicenne, 93000 Bobigny, France
5 Internal Medicine Department, AP-HP H?pital Pitié-Salpêtrière, 75013 Paris, France
6 Pierre and Marie Curie University, UPMC Paris Universitas, 75005 Paris, France
7 Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Agency, Kawaguchi 332-0012, Japan
8 WPI Immunology Frontier Research Center, Osaka University, Suita 565-0871, Japan
9 These authors contributed equally to this work
10 Present address: Internal Medicine Department and Institut National de la Santé et de la Recherche Médicale (INSERM) UMR-S 945, Laboratoire AP-HP d'immunologie cellulaire et tissulaire, H?pital Pitié-Salpêtrière, 75013 Paris, France
FoxP3 is a key transcription factor for the development and function of natural CD4+ regulatory Tcells (Treg cells). Here we show that human FoxP3+CD4+ Tcells were composed of three phenotypically and functionally distinct subpopulations: CD45RA+FoxP3lo resting Treg cells (rTreg cells) and CD45RAFoxP3hi activated Treg cells (aTreg cells), both of which were suppressive invitro, and cytokine-secreting CD45RAFoxP3lo nonsuppressive Tcells. The proportion of the three subpopulations differed between cord blood, aged individuals, and patients with immunological diseases. Terminally differentiated aTreg cells rapidly died whereas rTreg cells proliferated and converted into aTreg cells invitro and invivo. This was shown by the transfer of rTreg cells into NOD-scid-common -chain-deficient mice and by TCR sequence-based Tcell clonotype tracing in peripheral blood in a normal individual. Taken together, the dissection of FoxP3+ cells into subsets enables one to analyze Treg cell differentiation dynamics and interactions in normal and disease states, and to control immune responses through manipulating particular FoxP3+ subpopulations.
