國家衛生研究院 NHRI:Item 3990099045/2079
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    題名: Epstein-Barr virus (EBV) latent membrane protein-1 down-regulates tumor necrosis factor-alpha (TNF-alpha) receptor-1 and confers resistance to TNF-alpha-induced apoptosis in T cells - Implication for the progression to T-cell lymphoma in EBV-associated hemophagocytic syndrome
    其他題名: Epstein-Barr virus (EBV) latent membrane protein-1 down-regulates tumor necrosis factor-α (TNF-α) receptor-1 and confers resistance to TNF-α-induced apoptosis in T cells: implication for the progression to T-cell lymphoma in EBV-associated hemophagocytic syndrome
    作者: Chuang, HC;Lay, JD;Chuang, SE;Hsieh, WC;Chang, Y;Su, IJ
    貢獻者: Division of Clinical Research;National Institute of Cancer Research
    摘要: The infection of T cells by Epstein-Barr virus (EBV) may result in hemophagocytic syndrome (HPS) through enhanced cytokine secretion, particularly tumor necrosis factor-alpha (TNF-alpha), by EBV latent membrane protein-1 (LMP-1). One bewildering observation of HPS patients is relapsing disease or progression to T-cell lymphoma. This finding raises the question whether EBV LMP-1-expressing T cells may survive and proliferate in the cytokine milieu of HPS. To explore this possibility, we tested the sensitivity of LMP-1-expressing T cells to apoptosis in the presence of TNF-a. LMP-1 up-regulated TNF-alpha through TRAF2,5 and nuclear factor-kappa B pathway in T cells. The LMP-1-expressing T cells then became resistant to TN17-a-induced apoptosis. Interestingly, the expression of TNFR1 was remarkably down-regulated by LMP-1 in T cells. Furthermore, the TNF-alpha/TNFR1 downstream death signal TNFR1-associated death domain protein was constitutively recruited by LMP-1, and the activities of apoptotic caspases 3, 8, and 9 were suppressed. Reconstitution of TNFR1 successfully reversed the TNF-alpha-induced apoptotic cascades. Therefore, EBV LMP-1 not only activates T cells to proliferate but also confers resistance to TNF-alpha-mediated apoptosis via down-regulation of TNFR1 in the cytokine milieu of HPS. This finding provides a potential mechanism to explain the disease persistence or progression T-cell lymphoma HPS patients.
    關鍵詞: Pathology
    日期: 2007-05
    關聯: American Journal of Pathology. 2007 May;170(5):1607-1617.
    Link to: http://dx.doi.org/10.2353/ajpath.2007.061026
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0002-9440&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000246050400017
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=34250838092
    顯示於類別:[蘇益仁(2002-2015)] 期刊論文
    [張堯] 期刊論文
    [莊雙恩] 期刊論文
    [莊懷佳] 期刊論文

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