期刊
RHEUMATOLOGY
卷 51, 期 6, 页码 964-975出版社
OXFORD UNIV PRESS
DOI: 10.1093/rheumatology/ker402
关键词
FADD; rheumatoid arthritis; adenosine receptors; secretion; inflammation
类别
资金
- French Ministry of Tertiary Education and Research
- Ligue Contre le Cancer
- Arthritis Foundation
- Societe Francaise de Rhumatologie
- Ligue Contre le Cancer, Comite de Paris
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 kappa B (NF-kappa B), 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-kappa B activation.
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