國家衛生研究院 NHRI:Item 3990099045/11646
English  |  正體中文  |  简体中文  |  全文笔数/总笔数 : 12145/12927 (94%)
造访人次 : 907809      在线人数 : 934
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/3990099045/11646


    题名: Efficient uptake of recombinant lipidated survivin by antigen-presenting cells initiates antigen cross-presentation and antitumor immunity
    作者: Chiang, C;Wu, C;Liu, S;Leng, C;Chen, H
    贡献者: National Institute of Infectious Diseases and Vaccinology
    摘要: Background: Survivin is over-expressed in various types of human cancer, but rarely expressed in terminally differentiated adult tissues. Thus, survivin is a potential target antigen for a cancer vaccine. However, self-tumor associated antigens are not highly immunogenic. Bacteria derived lipoproteins can activate antigen-presenting cells through their toll-like receptors to enhance immune responses. In this context, lipidated survivin is an attractive candidate for cancer immunotherapy. Method: In the present study, recombinant lipidated human survivin (LSur) was prepared from an Escherichia coli-based system. We investigated whether LSur is efficiently captured by antigen presenting cells then facilitating effective induction of survivin cross-presentation and generation of immunity against cancer cells. Result: Our results demonstrate that LSur, but not its non-lipidated counterpart, can activate mouse bone marrow derived-dendritic cells (BMDCs) to enhance cytokine (IL-6, TNF-α, and IL-12) secretion and co-stimulatory molecules (CD40, CD80, CD86 and MHC II) expression. However, the pathways involved in the capture of the recombinant lipidated antigen by antigen-presenting cells have not yet been elucidated. To this end, we employ various endocytosis inhibitors to study the effect on LSur internalization. We show that the internalization of LSur is suppressed by the inhibition of various routes of endocytosis. These results suggest that endocytosis of LSur by BMDCs can be mediated by multiple mechanisms. Furthermore, LSur is trafficked to the early endosome after internalization by BMDCs. These features of LSur are advantageous for cross-presentation and the induction of antitumor immunity. Conclusion: We demonstrate that immunization of C57BL/6 mice with LSur under treatment with exogenous adjuvant-free formulation induce survivin-specific CD8+ T-cell responses and suppress tumor growth. The antitumor responses are mediated by CD8+ cells. Our findings indicate that LSur is a potential candidate for stimulating protective antitumor immunity. This study suggests that lipidated tumor antigens may be a promising approach for raising a robust antitumor response in cancer immunotherapy.
    日期: 2018-10
    關聯: Journal of Thoracic Oncology. 2018 Oct;13(10, Suppl.):S526.
    Link to: http://dx.doi.org/10.1016/j.jtho.2018.08.719
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=1556-0864&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000454014501352
    显示于类别:[陳信偉] 會議論文/會議摘要
    [冷治湘] 會議論文/會議摘要
    [劉士任] 會議論文/會議摘要

    文件中的档案:

    档案 描述 大小格式浏览次数
    ISI000454014501352.pdf137KbAdobe PDF257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