| Extracellular domain of human 4-1BBL enhanced the function of cytotoxic T-lymphocyte induced by dendritic cell. | |
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MedLine Citation:
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PMID: 21745658 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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Interaction of costimulatory molecules and their receptors is crucial for tumor lysate-pulsed dendritic cells (sensitized DC, sDC) to promote T cell activation, clonal expansion and its antitumor immunity. To augment the costimulatory signal may regulate the interaction between DC and cytotoxic T lymphocyte (CTL) and consequently enhance the antitumor response. The costimulatory ligand and receptor pair of 4-1BB/4-1BBL is one of the main factors in the costimulation of CTL. We explored the adjuvant role of a recombinant human 4-1BBL extracellular domain (ex4-1BBL) in modulating CTL activation induced by HepG2 antigen-loaded DC (sDC). The augment effects of sDC in combination with ex4-1BBL on the proliferation, activation, cell survival and cytotoxicity against HepG2 cells of CTL were examined. In the presence of ex4-1BBL, sDC exhibited markedly augmented effects on the above four functions of CTL. These results demonstrate that ex4-1BBL plays an important role in the costimulation pathway for DC-mediated CTL's activation, which might be a useful adjuvant factor for DC-based cancer biotherapy. |
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Authors:
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Chenxuan Wu; Hongxing Guo; Yijun Wang; Yingtang Gao; Zhengyan Zhu; Zhi Du |
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Publication Detail:
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Type: JOURNAL ARTICLE Date: 2011-6-23 |
Journal Detail:
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Title: Cellular immunology Volume: - ISSN: 1090-2163 ISO Abbreviation: - Publication Date: 2011 Jun |
Date Detail:
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Created Date: 2011-7-12 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 1246405 Medline TA: Cell Immunol Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Copyright Information:
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Copyright © 2011 Elsevier Inc. All rights reserved. |
Affiliation:
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Tianjin Third Central Hospital Affiliated to Tianjin Medical University, Tianjin Key Laboratory of Artificial Cells, 83 Jintang Road, Tianjin 300170, China. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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