调节性T细胞又称为抑制型T细胞，它在免疫系统复杂的调控机制中扮演了相当重要的角色。如今，研究人员发现了一种阻止调节性T细胞生产和功能的抑制信号环路，新成果发表在日前在线出版的《自然—免疫学》期刊上。
人体的免疫反应既要能迅速活化以抵御外来抗原的侵入，又要避免过度活化造成自身组织器官的损害，这是一个相当精致的平衡过程，调节性T细胞在其中发挥了重要作用，它通过抑制不需要的免疫反应来阻止自体免疫性疾病的发生，如糖尿病。
Hongbo Chi和同事发现，受体S1P1是这些调节性T细胞的关键抑制剂。在缺失S1P1的小鼠体内，调节性T细胞的数量增加了，它们具有更大的抑制性。相反，过度表达S1P1的小鼠出现了自体免疫疾病，因为调节T细胞基本上被消灭了。
这些最新的研究成果在临床上有相当的重要性，因为目前有试验因其他原因而正在对S1P1的功能进行调控。新研究发现了通过信号通道影响调节性T细胞的受体，拓展了我们对S1P1功能的认识。（生物谷Bioon.com）
生物谷推荐原始出处：
Nature Immunology 10, 769 - 777 (2009) 31 May 2009 | doi:10.1038/ni.1743
The receptor S1P1 overrides regulatory T cell–mediated immune suppression through Akt-mTOR
Guangwei Liu1, Samir Burns1, Gonghua Huang1, Kelli Boyd2, Richard L Proia3, Richard A Flavell4,5 & Hongbo Chi1,5
Regulatory T cells (Treg cells) are critically involved in maintaining immunological tolerance, but this potent suppression must be 'quenched' to allow the generation of adaptive immune responses. Here we report that sphingosine 1-phosphate (S1P) receptor type 1 (S1P1) delivers an intrinsic negative signal to restrain the thymic generation, peripheral maintenance and suppressive activity of Treg cells. Combining loss- and gain-of-function genetic approaches, we found that S1P1 blocked the differentiation of thymic Treg precursors and function of mature Treg cells and affected Treg cell–mediated immune tolerance. S1P1 induced selective activation of the Akt-mTOR kinase pathway to impede the development and function of Treg cells. Dynamic regulation of S1P1 contributed to lymphocyte priming and immune homeostasis. Thus, by antagonizing Treg cell–mediated immune suppression, the lipid-activated S1P1-Akt-mTOR pathway orchestrates adaptive immune responses.
1 Department of Immunology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA.
2 Animal Resources Center, St. Jude Children's Research Hospital, Memphis, Tennessee, USA.
3 Genetics of Development and Disease Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, USA.
4 Howard Hughes Medical Institute, New Haven, Connecticut, USA.
5 Department of Immunobiology, Yale University School of Medicine, New Haven, Connecticut, USA.
