Gondek David C, Lu Li-Fan, Quezada Sergio A, Sakaguchi Shimon, Noelle Randolph J
Department of Microbiology and Immunology, Dartmouth Medical School and Norris Cotton Cancer Center, Lebanon, NH 03756, USA.
J Immunol. 2005 Feb 15;174(4):1783-6. doi: 10.4049/jimmunol.174.4.1783.
CD4+CD25+ regulatory T cells (Treg) are potent immunosuppressive cells that are pivotal in the regulation of peripheral tolerance. In this report, we identify granzyme B (GZ-B) as one of the key components of Treg-mediated suppression. Induction of regulatory activity is correlated with the up-regulation of GZ-B expression. Proof of a functional involvement of GZ-B in contact-mediated suppression by Treg is shown by the reduced ability of Treg from GZ-B-/- mice to suppress as efficiently as Treg from WT mice. GZ-B-mediated suppression is perforin independent, because suppression by Treg from perforin-/- and WT is indistinguishable. Additionally, suppression mediated by Treg appears to be mediated, in part, by the induction of apoptosis in the CD4+CD25- effector cell. In summary, GZ-B is one of the key mechanisms through which CD4+CD25+ Treg induce cell contact-mediated suppression.
CD4+CD25+调节性T细胞(Treg)是强大的免疫抑制细胞,在调节外周免疫耐受中起关键作用。在本报告中,我们确定颗粒酶B(GZ-B)是Treg介导的抑制作用的关键组成部分之一。调节活性的诱导与GZ-B表达的上调相关。GZ-B-/-小鼠的Treg抑制能力低于野生型(WT)小鼠,这表明GZ-B在Treg接触介导的抑制中发挥功能性作用。GZ-B介导的抑制不依赖穿孔素,因为穿孔素-/-和WT小鼠的Treg抑制作用没有差异。此外,Treg介导的抑制似乎部分是通过诱导CD4+CD25-效应细胞凋亡来实现的。总之,GZ-B是CD4+CD25+ Treg诱导细胞接触介导的抑制作用的关键机制之一。