| Promoting immune responses by LIGHT in the face of abundant regulatory T cell inhibition. | |
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MedLine Citation:
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PMID: 20042587 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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CD4(+) regulatory T cell (Treg) populations are believed to play very important roles in the suppression of immune responses. Overriding Treg inhibition is necessary for initiating primary immune reaction upon inflammatory Ag stimulation. LIGHT, TNF superfamily member 14, has been shown to be a costimulatory molecule for effector T cells. Overexpression of lymphotoxin-related inducible ligand that competes for glycoprotein D binding to herpesvirus entry mediator on T cells (LIGHT) on T cells induces strong T cell-mediated experimental intestinal inflammation. How this process is initiated by LIGHT in suppressive intestinal environments remains incompletely understood. In this study, we assessed the effect of LIGHT on Tregs. Our results indicate that LIGHT can support the expansion and function of Tregs. However, when LIGHT was highly expressed, these abundant Tregs failed to suppress the development of T cell-mediated experimental colitis and antitumor immunity. We showed that this might be, in part, due to an ability of LIGHT to promote effector T cell proliferation and differentiation even in a Treg-abundant environment. Our data collectively suggest that LIGHT might be a critical cytokine involved in the development of autoimmune inflammatory diseases and that LIGHT-targeted immunotherapy might be useful in the treatment of these diseases. |
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Authors:
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Yugang Wang; Mingzhao Zhu; Ping Yu; Yang-Xin Fu |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural Date: 2009-12-30 |
Journal Detail:
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Title: Journal of immunology (Baltimore, Md. : 1950) Volume: 184 ISSN: 1550-6606 ISO Abbreviation: J. Immunol. Publication Date: 2010 Feb |
Date Detail:
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Created Date: 2010-01-21 Completed Date: 2010-03-12 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 2985117R Medline TA: J Immunol Country: United States |
Other Details:
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Languages: eng Pagination: 1589-95 Citation Subset: AIM; IM |
Affiliation:
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Department of Pathology, University of Chicago, Chicago, IL 60637, USA. yugang@uchicago.edu |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adoptive Transfer Animals CD4-Positive T-Lymphocytes / immunology, pathology, transplantation Cell Differentiation / genetics, immunology Cells, Cultured Colitis / genetics, immunology, pathology Homeodomain Proteins / genetics Immunosuppression* / methods Intestinal Mucosa / immunology, pathology Lymphocyte Activation / genetics, immunology Lymphopenia / genetics, immunology, pathology Mice Mice, Inbred C57BL Mice, Knockout Mice, Transgenic T-Lymphocytes, Regulatory / immunology*, metabolism, pathology Tumor Necrosis Factor Ligand Superfamily Member 14 / biosynthesis, genetics, physiology* |
| Grant Support | |
ID/Acronym/Agency:
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AI062026/AI/NIAID NIH HHS; CA115540/CA/NCI NIH HHS; DK58891/DK/NIDDK NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Homeodomain Proteins; 0/Tnfsf14 protein, mouse; 0/Tumor Necrosis Factor Ligand Superfamily Member 14; 128559-51-3/RAG-1 protein |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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