Howard Hughes Medical Institute and Department of Microbiology and Immunology, University of California, San Francisco, California 94143-0414, USA.
Annu Rev Immunol. 2012;30:69-94. doi: 10.1146/annurev-immunol-020711-075011. Epub 2011 Dec 5.
Much has been learned about how cells enter lymphoid tissues. But how do they leave? Sphingosine-1-phosphate (S1P) has emerged over the past decade as a central mediator of lymphocyte egress. In this review, we summarize the current understanding of how S1P promotes exit from the secondary lymphoid organs and thymus. We review what is known about additional requirements for emigration and summarize the mostly distinct requirements for exit from the bone marrow. Egress from lymphoid organs is limited during immune responses, and we examine how this regulation works. There is accumulating evidence for roles of S1P in directing immune cell behavior within lymphoid tissues. How such actions can fit together with the egress-promoting role of S1P is discussed. Finally, we examine current understanding of how FTY720, a drug that targets S1P receptors and is approved for the treatment of multiple sclerosis, causes immune suppression.
人们已经了解了细胞如何进入淋巴组织。但是它们是如何离开的呢?在过去的十年中,鞘氨醇-1-磷酸(S1P)已成为淋巴细胞迁出的主要介质。在这篇综述中,我们总结了目前对 S1P 如何促进次级淋巴器官和胸腺中细胞迁出的理解。我们回顾了已知的对迁出的其他要求,并总结了骨髓中细胞迁出的独特要求。在免疫反应期间,淋巴细胞从淋巴器官中的迁出受到限制,我们检查了这种调节机制的工作原理。越来越多的证据表明 S1P 在指导淋巴组织内免疫细胞行为方面发挥作用。讨论了这种作用如何与 S1P 的促进迁出作用相吻合。最后,我们研究了目前对 FTY720(一种靶向 S1P 受体的药物,已被批准用于治疗多发性硬化症)如何引起免疫抑制的理解。
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