國家衛生研究院 NHRI:Item 3990099045/6564
English  |  正體中文  |  简体中文  |  全文笔数/总笔数 : 12500/13673 (91%)
造访人次 : 2477129      在线人数 : 73
RC Version 6.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.
搜寻范围 查询小技巧：
  • 您可在西文检索词汇前后加上"双引号"，以获取较精准的检索结果
  • 若欲以作者姓名搜寻，建议至进阶搜寻限定作者字段，可获得较完整数据
    •  进阶搜寻
    主页 ‧ 登入 ‧ 上传 ‧ 说明 ‧ 关于NHRI ‧ 管理 到手机版


    jsp.display-item.identifier=請使用永久網址來引用或連結此文件: http://ir.nhri.org.tw/handle/3990099045/6564


    题名: CD4+ T cells disarm or delete cytotoxic T lymphocytes under IL-17–Polarizing conditions
    作者: Tsai, JP;Lee, MH;Hsu, SC;Chen, MY;Liu, SJ;Chang, JT;Liao, CT;Cheng, AJ;Chong, P;Chu, CL;Shen, CR;Chen, HW
    贡献者: Division of Vaccine Research and Development
    摘要: Previous studies have shown that TGF-β acts cooperatively with IL-6 to elicit a high frequency of IL-17–secreting CD4+ T cells (termed Th17) and an elevated CD8+IL-17+ T cell population (termed Tc17). These CD8+ cells fail to behave like most cytotoxic T lymphocytes that express IFN-γ and granzyme B, but they exhibit a noncytotoxic phenotype. Although a significant increase in the number of these Tc17 cells was found in tumors, their role and interaction with other cell types remain unclear. In this study, we demonstrate that the presence of CD4+CD25− T cells, but not the CD4+CD25+ (regulatory T [Treg]) cell population, significantly reduced the elicitation of Tc17 cells, possibly as a result of the induction of apoptotic signals. Importantly, these signals may be derived from soluble mediators, and the addition of anti–IL-2 restored the reduction of Tc17 cells in the presence of CD4+CD25− T cells. Finally, the elicited Tc17 and Treg cells exhibited a close association in patients with head and neck cancer, indicating that the surrounding Treg cells might maintain the survival of the Tc17 cells. Taken together, these results reveal an intriguing mechanism in which Tc17 cells are controlled by a finely tuned collaboration between the different types of CD4+ T cells in distinct tumor microenvironments.
    日期: 2012-08
    關聯: Journal of Immunology. 2012 Aug;189(4):1671-1679.
    Link to: http://dx.doi.org/10.4049/jimmunol.1103447
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0022-1767&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000307216000018
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84864813859
    显示于类别:[許素菁] 期刊論文
    [劉士任] 期刊論文
    [莊再成] 期刊論文
    [朱清良(2005-2007)] 期刊論文
    [陳信偉] 期刊論文

    文件中的档案:

    档案 描述 大小格式浏览次数
    PB2012072511.pdf2446KbAdobe PDF779检视/开启


    在NHRI中所有的数据项都受到原著作权保护.

    TAIR相关文章

    DSpace Software Copyright © 2002-2004  MIT &  Hewlett-Packard  /   Enhanced by   NTU Library IR team Copyright ©   - 回馈