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IL-12 and IL-23 Production in Toxoplasma gondii- or LPS-Treated Jurkat T Cells via PI3K and MAPK Signaling Pathways

  • Ismail, Hassan Ahmed Hassan Ahmed (Department of Infection Biology, Chungnam National University School of Medicine) ;
  • Kang, Byung-Hun (Department of Obstetrics and Gynecology, Chungnam National University School of Medicine) ;
  • Kim, Jae-Su (Department of Infection Biology, Chungnam National University School of Medicine) ;
  • Lee, Jae-Hyung (Department of Infection Biology, Chungnam National University School of Medicine) ;
  • Choi, In-Wook (Department of Infection Biology, Chungnam National University School of Medicine) ;
  • Cha, Guang-Ho (Department of Infection Biology, Chungnam National University School of Medicine) ;
  • Yuk, Jae-Min (Department of Infection Biology, Chungnam National University School of Medicine) ;
  • Lee, Young-Ha (Department of Infection Biology, Chungnam National University School of Medicine)
  • Received : 2017.07.11
  • Accepted : 2017.11.24
  • Published : 2017.12.31

Abstract

IL-12 and IL-23 are closely related in structure, and have been shown to play crucial roles in regulation of immune responses. However, little is known about the regulation of these cytokines in T cells. Here, we investigated the roles of PI3K and MAPK pathways in IL-12 and IL-23 production in human Jurkat T cells in response to Toxoplasma gondii and LPS. IL-12 and IL-23 production was significantly increased in T cells after stimulation with T. gondii or LPS. T. gondii and LPS increased the phosphorylation of AKT, ERK1/2, p38 MAPK, and JNK1/2 in T cells from 10 min post-stimulation, and peaked at 30-60 min. Inhibition of the PI3K pathway reduced IL-12 and IL-23 production in T. gondii-infected cells, but increased in LPS-stimulated cells. IL-12 and IL-23 production was significantly reduced by ERK1/2 and p38 MAPK inhibitors in T. gondii- and LPS-stimulated cells, but not in cells treated with a JNK1/2 inhibitor. Collectively, IL-12 and IL-23 production was positively regulated by PI3K and JNK1/2 in T. gondii-infected Jurkat cells, but negatively regulated in LPS-stimulated cells. And ERK1/2 and p38 MAPK positively regulated IL-12 and IL-23 production in Jurkat T cells. These data indicate that T. gondii and LPS induced IL-12 and IL-23 production in Jurkat T cells through the regulation of the PI3K and MAPK pathways; however, the mechanism underlying the stimulation of IL-12 and IL-23 production by T. gondii in Jurkat T cells is different from that of LPS.

Keywords

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