Stromal cell-derived factor 1 alpha-induced chemotaxis in T cells is mediated by nitric oxide signaling pathways.
作者： Rama P. Cherla , Ramesh K. Ganju
DOI: 10.4049/JIMMUNOL.166.5.3067
关键词:
摘要: Stromal cell-derived factor 1 alpha (SDF1 alpha) and its cognate chemokine receptor CXCR4 act as potent chemoattractants regulate trafficking homing of hematopoietic progenitor cells lymphocytes. However, the molecular mechanisms regulating SDF1 alpha-driven cell migration are not well defined. In this study, we have explored roles second messenger NO transcription NF-kappa B in alpha-induced T migration. treatment Jurkat increased activity synthase, which catalyzes generation NO. We observed that pretreatment or activated PBLs with several donors significantly enhanced migration, whereas various inhibitors synthase markedly abrogated chemotactic response a concentration-dependent manner. Furthermore, B, is linked to signaling pathways, also blocked response. these compounds did significant effect on mitogen-activated protein kinase activity. addition, MAP/Erk inhibitor PD98059 abrogate chemotaxis. AKT, has been shown mediate production, was phosphorylated upon stimulation. These studies suggest NO-related pathways may chemotaxis, but activation.
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