Nanki T, Lipsky P E
National Institute of Arthritis and Musculoskeletal and Skin Diseases, Bethesda, Maryland 20892-1820, USA.
Cell Immunol. 2001 Dec 15;214(2):145-54. doi: 10.1006/cimm.2001.1890.
Recently we found that CXCL12/SDF-1 is a costimulator of peripheral CD4+ T cells. In this study, we report that CXCL12 alone induced expression of activation markers by peripheral CD4+ memory T cells and costimulated activation marker expression by anti-CD3 stimulated peripheral CD4+ naive and CD4+ memory T cells as well as by peripheral CD8+ T cells. The stimulation by CXCL12 was inhibited by Pertussis Toxin (PTX), but not by anti-CD25 mAb. CXCL12 also induced enhancement of IL-2 production and proliferation by anti-CD3 stimulated CD4+ memory T cells, but not by CD4+ naive T cells. PTX inhibited the enhancement of IL-2 production and proliferation, whereas anti-CD25 mAb inhibited proliferation, but not IL-2 production. Thus, CXCL12 upregulated T-cell activation, and a G-coupled protein mediated signaling pathway was necessary for stimulation of T cells by CXCL12.
最近我们发现，CXCL12/SDF-1是外周CD4+T细胞的共刺激因子。在本研究中，我们报告单独的CXCL12可诱导外周CD4+记忆T细胞表达激活标志物，并协同刺激抗CD3刺激的外周CD4+初始T细胞、CD4+记忆T细胞以及外周CD8+T细胞表达激活标志物。百日咳毒素（PTX）可抑制CXCL12的刺激作用，但抗CD25单克隆抗体则无此作用。CXCL12还可诱导抗CD3刺激的CD4+记忆T细胞增强IL-2产生和增殖，但对CD4+初始T细胞无此作用。PTX可抑制IL-2产生和增殖的增强，而抗CD25单克隆抗体可抑制增殖，但不抑制IL-2产生。因此，CXCL12上调T细胞激活，且G偶联蛋白介导的信号通路对于CXCL12刺激T细胞是必需的。
Zotero 插件