期刊
TUMORI JOURNAL
卷 97, 期 3, 页码 350-357出版社
SAGE PUBLICATIONS LTD
DOI: 10.1177/030089161109700316
关键词
human NK cells; NKG2D; TGF-beta; DAP10; tumor immunity
类别
资金
- Korea Health 21 RD Project [A050564, A062260]
- Ministry of Health & Welfare, Republic of Korea [0320020-2]
- Korea Health Promotion Institute [A062260] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Aims and background. Elevated TGF-beta 1 secretion and down-modulation of NKG2D underlies impaired NK cytotoxicity in cancer patients. However, the molecular mechanism of immunosuppression by TGF-beta 1 is not yet clarified. Methods. IL-2-activated human NK cells were cultured with TGF-beta 1. Protein levels of NKG2D and DAP10 were examined by FAGS or immunoblot analyses. Real-time RTPCR was performed to quantify the transcription levels. MAPK inhibitors were used to investigate intracellular signaling. Results. TGF-beta 1 down-regulated total and surface NKG2D, which was partially dependent on transcriptional regulation. TGF-beta 1 treatment of human NK cells resulted in significant changes in both transcriptional and translational levels of DAP10. Moreover, treatment with bafilomycin A1 or folimycin restored total NKG2D levels in TGF-beta 1-treated NK cells. The impaired NKG2D down-modulation by TGF-beta 1 was not associated with activation of the MAPK signaling pathway. Conclusions. TGF-beta 1 down-modulates surface NKG2D expression by controlling the transcriptional and translational levels of DAP10.
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