2007
DOI: 10.1002/art.22494
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Decoy receptor 3 expressed in rheumatoid synovial fibroblasts protects the cells against fas‐induced apoptosis

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Cited by 74 publications
(70 citation statements)
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“…17 Human renal interstitial fibroblasts constitutively express Fas and are susceptible to Fas-induced apoptosis. 19 Hayashi et al 18 found that TNFRSF6B offers a survival benefit to synovial fibroblasts in terms of protection against cytotoxic and regulatory effects of Fas. In accordance with these findings, we also showed that TNFRSF6B could protect renal myofibroblasts against Fas-induced apoptosis (Supplementary Figure S1).…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…17 Human renal interstitial fibroblasts constitutively express Fas and are susceptible to Fas-induced apoptosis. 19 Hayashi et al 18 found that TNFRSF6B offers a survival benefit to synovial fibroblasts in terms of protection against cytotoxic and regulatory effects of Fas. In accordance with these findings, we also showed that TNFRSF6B could protect renal myofibroblasts against Fas-induced apoptosis (Supplementary Figure S1).…”
Section: Discussionmentioning
confidence: 99%
“…17 Anti-apoptotic effect of TNFRSF6B has been shown to decrease elimination of rheumatoid synovial fibroblasts by blocking the interaction with Fas ligand. 18 Fas is normally expressed in human renal interstitial fibroblasts 19 and we hypothesize that TNFRSF6B could involve in the renal fibrogenesis. Therefore, it prompts us to investigate whether TNFRSF6B is pathologically expressed in the kidney tissues of patients with chronic kidney disease, and to appraise whether expression of TNFRSF6B in kidneys is a newer tissue biomarker for prediction of disease progression.…”
mentioning
confidence: 85%
“…Although other mechanisms, including upregulation of inflammatory cytokines and/or interaction with other ligands, can occur as well, our evidences are consistent with literature data reporting that DcR3 can bind FasL, and may act as an inhibitor of FasL-induced cell death. 15,16,30 This is an important point considering that FasL-mediated apoptosis is the most common physiological form of cell death, and occurs during embryonic development, tissue remodeling, immune regulation and tumor regression. Abnormalities in the FasL system and the overexpression of DcR3 associated with a resistance to FasLmediated apoptosis can result in a number of human pathological conditions, including tumors.…”
Section: Discussionmentioning
confidence: 99%
“…[4] DcR3 exerts pleiotropic roles as a decoy receptor by an anti-apoptotic activity and a non-decoy receptor by its direct immune-modulatory properties. Recent studies have shown that DcR3 is up-regulated and may be pathogenetically implicated in sepsis and diverse chronic inflammatory diseases.…”
Section: Discussionmentioning
confidence: 99%
“…[4] The role of DcR3 in infection has been studied in depth. [5] , had analyzed DcR3 mRNA levels in purified cell populations obtained from peripheral blood mononuclear cell (PBMC) from healthy donors by quantitative reverse transcriptase polymerase chain reaction (qRT-PCR).…”
Section: Introductionmentioning
confidence: 99%