| Fas-associated death domain protein and adenosine partnership: fad in RA. | |
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MedLine Citation:
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PMID: 22253026 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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Inflammation is the principal hallmark of RA. Different pathways are implicated in the production of pro-inflammatory cytokines, the bona fide mediators of this inflammation. Among them are the TNF pathway and the IL-1 receptor/Toll-like receptor (IL-1R/TLR4) pathway. One of the potential negative regulators of IL-1R/TLR4 signalling is the Fas-associated death domain protein (FADD), which is the pivotal adaptor of the apoptotic signal mediated by death receptors of the TNF family. FADD can sequester myeloid differentiation primary response gene 88 (MyD88), the common adaptor of most TLRs, and hence hinder the activation of nuclear factor κB (NF-κB), the downstream transcription factor. We recently described a new regulatory mechanism of FADD expression, via the shedding of microvesicles, mediated by adenosine receptors. Interestingly, adenosine is found in high concentrations in the joints of RA patients and has been largely reported as a regulator of inflammation. This review discusses the possible link that could exist between the adenosine-dependent regulation of FADD in the inflammatory context of RA and the potential role of FADD as a therapeutic target in the treatment of RA. We will see that the modulation of FADD expression may be a double-edged sword by increasing apoptosis and at the same time limiting NF-κB activation. |
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Authors:
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Valérie Vilmont; Léa Tourneur; Gilles Chiocchia |
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Publication Detail:
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Type: JOURNAL ARTICLE Date: 2012-1-16 |
Journal Detail:
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Title: Rheumatology (Oxford, England) Volume: - ISSN: 1462-0332 ISO Abbreviation: - Publication Date: 2012 Jan |
Date Detail:
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Created Date: 2012-1-18 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 100883501 Medline TA: Rheumatology (Oxford) Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Affiliation:
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Département d'Immunologie-Hématologie, Institut Cochin, Inserm U1016, Department Immunologie Hématologie, CNRS, UMR 8104, Department Immunologie-Hématologie, Université Paris Descartes, Sorbonne Paris Cité, Paris and Service de Rhumatologie, Hôpital Ambroise Paré, Boulogne, France. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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