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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2003.1
- 수록면
- 175 - 180 (6page)
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초록· 키워드
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Earlier study showed that glucocorticoid induced tumor necrosis factor receptor (GITR), a new TNFR family, activated murine macrophages to expres inducible nitric oxide synthase (iNOS) and to generate nitric oxide (NO). A possible involvement of pro-inflamatory cytokines on NO production by GITR was investigated in vitro systems and signaling molecules contributing to sGITR-induced cels, a murine macrophage cell line. The result showed that the synergy was afforded by the combination of GITR with IFN-γ in a dose-de-pendent maner but IFN-γ alone was not able to induce NOS. No effects were observed with TNF-α, IL-1β, or IL-6 co-treated with GITR. To determine signaling molecules contributing to sGITR-induced iNOS production, a specific inhibitor for signal pathway proteins tested showed that PDTC (NF- κB) and genistein (tyrosine kinase) inhibited NOS date (tyrosine phosphatase) potentiated NOS ex-pression. These results sugest that activations of NF-κB were involved in induction of iNOS by GITR and IFN-γ priming caused earlier and stronger NF- κB activation.
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