Th22 cells play a crucial part in pathogenesis of autoimmune diseases.H owever,little is known about a mechanistic process of regulating their *** this study,Jagged-1 signaling suppressed the deviation of naive CD4+T ...
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Th22 cells play a crucial part in pathogenesis of autoimmune diseases.H owever,little is known about a mechanistic process of regulating their *** this study,Jagged-1 signaling suppressed the deviation of naive CD4+T cells into Th22,which could be rescued by DAPT or hes-1 ***-1 contributed to the reduction of Th22 by lessening AHR level,but the knockdown of arnt or ahr could facilitate Th22 *** were the significant interactions among Hes-1,AHR level and ARNT,whereas their up-or down-stream relationships were confirmed by various ***-1 signaling markedly alleviated the joint swelling and clinical scores in the rheumatoid arthritis-bearing mice via the diminished Th22 with the inhibition of TNF-α and *** findings strongly indicate that the activated Jagged-1/Notch pathway suppresses the skewing of naive CD4T cells into Th22 to relieve rheumatoid arthritis through reduction of IL-22 and TNF-α by Hes-1/ARNT/AHR signaling.
Our previous results proved that Jagged-1/Notch signaling inhibits the phenotypic transformation of naive CD4+T cells into Th22 induced by both IL-6 and TNF-α.The current study showed that this process was facilitate...
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Our previous results proved that Jagged-1/Notch signaling inhibits the phenotypic transformation of naive CD4+T cells into Th22 induced by both IL-6 and TNF-α.The current study showed that this process was facilitated by hsp90 knockdown or SNX2112 with the augment of il-22,ahr and arnt,the attenuation of hes-1 as well as the high productions of Th22 cytokines and CCR6,which could be reversed by Hsp90 overexpression or *** Jagged-1 or DAPT caused downregulation or upregulation of Th22 phenotype,no changes were observed at the levels of Hsp90 mRNA and ***,the inhibition or activation of Hsp90 was able to reduce or enhance downstream Hes-1 via interacting with NICD and *** in vivo overexpression of Hsp90 could suppress deviation of Th22,which were rescued by hsp90 *** data demonstrate that Hsp90 can stabilize NICD and AhR to boost Notch signaling transduction,suggesting that it regulates Notch signaling to mediate Th22 differentiation.
目的探讨下调αB-晶状体蛋白(αB-crystallin)对人皮肤角质形成细胞(Ha Ca T)在应激条件下的存活和凋亡的影响。方法设计并筛选特异性靶向下调αB-crystallin表达的siRNA;噻唑蓝法检测siRNA下调αB-crystallin表达对过氧化氢(H2O2)处理...
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目的探讨下调αB-晶状体蛋白(αB-crystallin)对人皮肤角质形成细胞(Ha Ca T)在应激条件下的存活和凋亡的影响。方法设计并筛选特异性靶向下调αB-crystallin表达的siRNA;噻唑蓝法检测siRNA下调αB-crystallin表达对过氧化氢(H2O2)处理的细胞相对存活率的影响;流式细胞术检测siRNA下调αB-晶状体蛋白表达对H2O2诱导的细胞凋亡率的影响。结果筛选获得可有效下调αB-crystallin表达的siRNA(si-CRYAB-1);si-CRYAB-1下调αB-crystallin表达可降低H2O2处理后的Ha Ca T细胞存活率(P<0.01),并明显增加H2O2诱导的Ha Ca T细胞凋亡率(P<0.05)。结论下调αB-crystallin的表达后,人角质形成细胞在氧化应激条件下的存活能力明显减弱。αB-crystallin可能具有抗人角质形成细胞凋亡的作用。
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