Role of JAK2/STAT5/Foxp3 signaling pathway in Jurkat T cells secretion of cytokines induced by traffic-related PM 2.5 and different components

Abstract

Abstract Studies have shown that traffic-related PM2.5 (TRPM2.5) can damage the immune system and reduce resistance to various diseases. However, the specific mechanisms remain unclear. In this study, Jurkat T cells were used as immune cells model. Exposure to different concentrations of TRPM2.5, water-soluble ions (WSI), and organic extract (OE) aggravated the inflammation of Jurkat T cells, increased the mRNA and protein expressions of JAK2 (Janus kinase 2), reduced signal transducer and activator of transcription (STAT5) and forkhead box P3 (Foxp3), decreased the proportions of Treg cells, and then diminished the release of cytokine IL-10 and TGF-β. However, after AG490 treatment, JAK2 and p-JAK2 mRNA and protein levels were inhibited, and STAT5 and Foxp3 mRNA and protein expressions were improved. Moreover, after transfection with STAT5 plasmid, the mRNA and protein expression of STAT5 and Foxp3 was significantly enhanced. Therefore, JAK2/STAT5/Foxp3 signaling pathway may play a critical regulatory role in the alteration of inflammatory mediators of Jurkat T cells induced by TRPM2.5 and its different components, which provides a scientific reference for the immune-inflammatory diseases caused by PM2.5.