Interleukin-18 induces activation and association of p56(lck) and MAPK in a murine TH1 clone.
Interleukin-18 (IL-18) was identified as an inducer of interferon-gamma (IFN-gamma) production by stimulated T cells. In this study, we used an ovalbumin-responsive murine Th1 clone (OVA#4), in which DNA synthesis was reportedly enhanced after IL-18 treatment in the presence of a non-mitogenic TCR/ CD3 stimulus, to examine signal transduction pathways. In the presence of the stimulus, IL-18 induced the appearance of tyrosine-phosphorylated proteins and herbimycin A inhibited DNA synthesis. It is suggested that protein tyrosine kinase (PTK) mediated signaling is induced by IL-18. Specifically, IL-18 induced phosphorylation of phosphorylates p56(lck) (LCK) and mitogen-activated protein kinase ( MAPK). IL-18 alone induced the kinase activities of both LCK and MAPK, and the activities were increased by the TCR/ CD3 stimulus. Simultaneously, IL-18 induced the association of LCK with MAPK and this was also increased by the TCR/ CD3 stimulus. The activation of the LCK- MAPK pathway correlated with enhanced DNA synthesis in OVA#4 cells. These results suggest that the LCK- MAPK pathway is involved in IL-18 signaling and that IL-18 may play an important role in modification of TCR/ CD3-mediated response.[1]References
- Interleukin-18 induces activation and association of p56(lck) and MAPK in a murine TH1 clone. Tsuji-Takayama, K., Matsumoto, S., Koide, K., Takeuchi, M., Ikeda, M., Ohta, T., Kurimoto, M. Biochem. Biophys. Res. Commun. (1997) [Pubmed]
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