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The Journal of Immunology, 1998, 161: 3624-3630.
Copyright © 1998 by The American Association of Immunologists

Stem Cell Factor Augments Fc{epsilon}RI-Mediated TNF-{alpha} Production and Stimulates MAP Kinases via a Different Pathway in MC/9 Mast Cells1

Tamotsu Ishizuka*,{dagger}, Hideki Kawasome*,{dagger}, Naohiro Terada*,{dagger}, Katsuyuki Takeda*,{dagger}, Pär Gerwins*,{dagger}, Gordon M. Keller{ddagger}, Gary L. Johnson*,{dagger} and Erwin W. Gelfand2,*,{dagger}

* Division of Basic Sciences, Department of Pediatrics, {dagger} Program in Molecular Signal Transduction, and {ddagger} Division of Immunology, Department of Medicine, National Jewish Medical and Research Center, Denver, CO 80206

Mast cells express the receptor tyrosine kinase kit/stem cell factor receptor (SCFR) which is encoded by the proto-oncogene c-kit. Ligation of SCFR induces its dimerization and activation of its intrinsic tyrosine kinase activity leading to activation of Raf-1, phospholipases, phosphatidylinositol 3-kinase, and extracellular signal-regulated kinases. However, little is known about the downstream signals initiated by SCFR ligation except for activation of extracellular signal-regulated kinases. The murine mast cell line, MC/9, synthesizes and secretes TNF-{alpha} following the aggregation of high affinity Fc receptors for IgE (Fc{epsilon}RI). Ligation of SCFR or Fc{epsilon}RI on MC/9 cells resulted in the activation of all three MAP kinase family members, extracellular signal-regulated kinases, c-Jun amino-terminal kinase (JNK), and p38. Stem cell factor (SCF)-induced activation of JNK and p38 was insensitive to wortmannin, cyclosporin A, and FK506 whereas activation of these kinases through Fc{epsilon}RI was sensitive to these drugs. Coligation of SCFR augmented Fc{epsilon}RI-mediated activation of MAP kinases, especially JNK activation, and SCF augmented Fc{epsilon}RI-mediated TNF-{alpha} production in MC/9 cells, although SCF alone did not induce TNF-{alpha} production. This augmentation by SCF was regulated at the level of transcription, at least in part, since the promoter activity of TNF-{alpha} was enhanced following addition of SCF. These results demonstrate that SCF can augment Fc{epsilon}RI-mediated JNK activation and cytokine gene transcription but via pathways that are regulated differently than the ones activated through Fc{epsilon}RI.




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