| The role of TWEAK/Fn14 in the pathogenesis of inflammation and systemic autoimmunity. | |
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MedLine Citation:
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PMID: 15353286 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Interactions between members of the TNF ligand superfamily with their cognate TNF receptors play a crucial role in maintaining immune homeostasis in normal individuals, while dysregulation of certain TNF-ligands and receptors contributes to the pathogenesis of autoimmunity. Identification of novel members of the TNF ligand and receptor families will promote our understanding of the pathogenesis of systemic autoimmune diseases, thus facilitating the development of novel therapeutic approaches. TNF-like weak inducer of apoptosis (TWEAK), a recently identified member of the TNF ligand family, induces PGE2, MMP-1, IL-6, IL-8, RANTES, and IP-10 in fibroblasts and synoviocytes, and upregulates ICAM-1, E-selectin, IL-8, and MCP-1 in endothelial cells. The receptor for TWEAK, Fn14, is expressed in various organs including the kidney; it is intriguing that some of these chemokines induced by TWEAK are crucial in the pathogenesis of lupus nephritis. Furthermore, others have described upregulated TWEAK expression on the surface of T cells in human lupus. In this paper we review the possible roles of TWEAK/TWEAK receptor interactions in the pathogenesis of inflammatory and systemic autoimmune diseases, with particular focus on systemic lupus erythematosus. TWEAK blockade may be helpful therapeutically in restoration of tolerance, but is more likely to modify inflammatory damage in target organs. |
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Authors:
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Sean Campbell; Jennifer Michaelson; Linda Burkly; Chaim Putterman |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review Date: 2004-09-01 |
Journal Detail:
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Title: Frontiers in bioscience : a journal and virtual library Volume: 9 ISSN: 1093-4715 ISO Abbreviation: Front. Biosci. Publication Date: 2004 Sep |
Date Detail:
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Created Date: 2004-09-08 Completed Date: 2006-09-28 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 9709506 Medline TA: Front Biosci Country: United States |
Other Details:
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Languages: eng Pagination: 2273-84 Citation Subset: IM |
Affiliation:
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The Department of Microbiology and Immunology, Albert Einstein College of Medicine, 1300 Morris Park Ave., Bronx, NY 10461, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Apoptosis Autoimmune Diseases / metabolism* Autoimmunity* Cell Membrane / metabolism Endothelium, Vascular / cytology, metabolism Humans Inflammation / metabolism* Ligands Lupus Erythematosus, Systemic / metabolism Lupus Nephritis / metabolism Multigene Family Receptors, Tumor Necrosis Factor / physiology* Signal Transduction Tumor Necrosis Factors / metabolism, physiology* |
| Grant Support | |
ID/Acronym/Agency:
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P01-A1-51392//PHS HHS; R01-AR-48692/AR/NIAMS NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Ligands; 0/Receptors, Tumor Necrosis Factor; 0/TNFSF12 protein, human; 0/TWEAK receptor; 0/Tnfsf12 protein, mouse; 0/Tumor Necrosis Factors |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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