EEQG est inventépar professeur Dekun Wang of shanxi institut de médecin chinoise traditionnelle et est mieux recherchéet développépar professeur Baoyun Yan et Qingrui Liu etc,de vice réda...EEQG est inventépar professeur Dekun Wang of shanxi institut de médecin chinoise traditionnelle et est mieux recherchéet développépar professeur Baoyun Yan et Qingrui Liu etc,de vice rédacteur en chef de journal de moderne electrophysiologie et produit par Tianjin Hede sciences et techniques et développement sociétéanonyme.Il est produit premier dans notre gays et展开更多
Rheumatoid arthritis(RA)is exacerbated by TNF-alpha signaling.However,it remains unclear whether TNF-α-activated TNFR1 and TNFR2 are regulated by extracellular factors.Here,we showed that soluble glycosylated interle...Rheumatoid arthritis(RA)is exacerbated by TNF-alpha signaling.However,it remains unclear whether TNF-α-activated TNFR1 and TNFR2 are regulated by extracellular factors.Here,we showed that soluble glycosylated interleukin-17 receptor D(sIL-17RD),which was produced by proteolytic cleavage,enhanced TNF-α-induced RA.We revealed that IL-17RD shedding was induced by the proteolytic enzyme TACE and enhanced by TNF-αexpression in macrophages.Intriguingly,sIL-17RD was elevated in the sera of arthritic mice and rats.Recombinant sIL-17RD significantly enhanced the TNF-α-induced proinflammatory response by promoting TNF-α-TNFR-sIL-17RD complex formation and receptor clustering,leading to the accelerated development of collagen-induced arthritis.Our observations revealed that ectodomain shedding of IL-17RD occurred in RA to boost the TNF-α-induced inflammatory response.Targeting sIL-17RD may provide a new strategy for the therapy of RA.展开更多
文摘EEQG est inventépar professeur Dekun Wang of shanxi institut de médecin chinoise traditionnelle et est mieux recherchéet développépar professeur Baoyun Yan et Qingrui Liu etc,de vice rédacteur en chef de journal de moderne electrophysiologie et produit par Tianjin Hede sciences et techniques et développement sociétéanonyme.Il est produit premier dans notre gays et
基金This work was supported by grants from the Chinese National Major Scientific Research Program(2016YFA0500301)from the National Natural Science Foundation of China(NSFC)(81872244,81830092,and 81572729).
文摘Rheumatoid arthritis(RA)is exacerbated by TNF-alpha signaling.However,it remains unclear whether TNF-α-activated TNFR1 and TNFR2 are regulated by extracellular factors.Here,we showed that soluble glycosylated interleukin-17 receptor D(sIL-17RD),which was produced by proteolytic cleavage,enhanced TNF-α-induced RA.We revealed that IL-17RD shedding was induced by the proteolytic enzyme TACE and enhanced by TNF-αexpression in macrophages.Intriguingly,sIL-17RD was elevated in the sera of arthritic mice and rats.Recombinant sIL-17RD significantly enhanced the TNF-α-induced proinflammatory response by promoting TNF-α-TNFR-sIL-17RD complex formation and receptor clustering,leading to the accelerated development of collagen-induced arthritis.Our observations revealed that ectodomain shedding of IL-17RD occurred in RA to boost the TNF-α-induced inflammatory response.Targeting sIL-17RD may provide a new strategy for the therapy of RA.
