【摘 要】
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OBJECTIVE;The interleukin (IL)-12 cytokine family is closely related to the development of T helper cells,which are responsible for autoimmune disease enhancement or suppression.IL-12 family members are generally heterodimers and share three α-subunits(p3
【机 构】
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The Rheumatism Research Center,The Catholic University of Korea,Seoul,South Korea;Division of Rheuma
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OBJECTIVE;The interleukin (IL)-12 cytokine family is closely related to the development of T helper cells,which are responsible for autoimmune disease enhancement or suppression.IL-12 family members are generally heterodimers and share three α-subunits(p35,p19,and p28) and two β-subunits (p40 and EBI3).However,a β-sheet p40 homodimer has been shown to exist and antagonize IL-12 and IL-23 signaling 1.Therefore,we assumed the existence of a p40-EBI3 heterodimer in nature and sought to investigate its role in immune regulation.METHODS;The presence of the p40-EBI3 heterodimer was confirmed by ELISA,immunoprecipitation,and western blotting.A p40-EBI3 vector and p40-EBI3-Fc protein were synthesized to confirm the immunological role of this protein in mice with collagen-induced arthritis (CIA).The anti-inflammatory effects of p40-EBI3 were analyzed with regard to clinical,histological,and immune cell-regulating features in mice with ClA.RESULTS:Clinical arthritis scores and the expression levels of proinflammatory cytokines (e.g.,IL-17,IL-13,IL-6,and TNF-α)were significantly attenuated in p40-EBI3-overexpressing and p40-EBI3-Fc-treated mice with ClA compared to vehicle-treated mice with CIA.Structural joint damage and vessel formation-related gene expression were also reduced by p40-EBI3 heterodimer treatment.In vitro,the p40-EBI3-Fc protein significantly suppressed the differentiation of Th17 cells and reciprocally induced CD4+CD25+Foxp3+ (regulatory T) cells.p40-EBI3 also inhibited osteoclast formation in a concentration-dependent manner.CONCLUSION:In this study,p40-EBI3 ameliorated proinflammatory conditions both in vivo and in vitro.We propose that p40-EBI3 is a novel anti-inflammatory cytokine involved in suppressing the immune response through the expansion of Treg cells and suppression of Th17 cells and osteoclastogenesis.
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