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.
粉尘螨是诱导过敏性疾病的重要变应原,可诱发Ⅰ型变态反应,对其免疫原性的鉴定是研究过敏性鼻炎等过敏性疾病的基础.首次对粉尘螨过敏原基因Der f 35进行克隆表达、纯化及免疫原性鉴定,提取粉尘螨总核糖核酸(ribonucleic acid,RNA),根...
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粉尘螨是诱导过敏性疾病的重要变应原,可诱发Ⅰ型变态反应,对其免疫原性的鉴定是研究过敏性鼻炎等过敏性疾病的基础.首次对粉尘螨过敏原基因Der f 35进行克隆表达、纯化及免疫原性鉴定,提取粉尘螨总核糖核酸(ribonucleic acid,RNA),根据已知基因序列(GenBank:LC175222.1)设计引物进行反转录聚合酶链式反应扩增,经Bam H I和Xho I双酶切,连接构建pET-32a-Der f 35载体,并克隆至大肠杆菌TOP 10菌株,取1 mL克隆菌液进行测序.使用试剂盒提取高纯度质粒转至感受态细胞Rosetta(DE3)中进行诱导、表达纯化及免疫学鉴定,并进行同源性比对分析、进化树构建及二级结构预测.克隆和表达结果显示,Der f 35基因的片段长约436个碱基对(base pair,bp);重组蛋白Der f 35相对分子质量约为30 ku(1 u=1 D),与预期结果相符.蛋白质印迹法结果证明,Der f 35与尘螨过敏性疾病患者的血清结合有明显的反应原性.生物信息学进化树结果显示,粉尘螨与屋尘螨、热带无爪螨、害嗜鳞螨、绵羊痒螨和免耳痒螨亲缘关系较近,二级结构预测显示Der f 35的氨基酸序列由2个α螺旋、6个β折叠、2个β转角和10个无规则卷曲片段组成.研究结果可为尘螨过敏性疾病的诊断与治疗提供理论依据.
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