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第九届全国免疫学学术大会

作者： Jie LIANG Wen ZHANG Shi-Jin WANG Li WANG Wen-Chao ZHOU Xiao GENG Bei ZHANG Department of Immunology Medical College of Qingdao University

Background:Hepatitis B virus(HBV)is the most common hepatitis virus that can cause acute and chronic infection of liver in *** infection may progress to liver cirrhosis and,eventually,hepatocellular *** do not directly cause liver cell injury,once the HBV infection is established,the outcomes are closely related to the coordinated responses of humoral and cellular *** immune response can lead to viral clearance and recovery,but excess immune response can lead to liver failure,and inadequate immune response will result in sustained HBV *** balance between th1/th2 cells is likely important in influencing the clinical outcome and disease progression of HBV infection ***,the th1/th2 dichotomy has been revisited and two additional subsets,the IL-17-producing subset(th17)and forkhead box P3(FoxP3)positive regulatory subset(Treg)have been *** 7 cells are important in defensing against a number of microorganisms,while Treg display a suppressive function in immune responses and inflammatory *** balance between th17 and Treg cells has been proved in immune ***,there variations are still not clear in the progression of HBV-related liver ***:to study the balance between th17 and Treg cells in the development of acute and chronic hepatic ***:this study consisted of 35 acute hepatitis B(AHB)patients,28 HBV-related liver fibrosis(HBV-LF)patients and 23 healthy controls(HC).Treg and th17 cells differentiation related cytokine levels were detected by enzyme-linked immuno sorbent assay(ELISA),and the frequency of Treg and th17 in peripheral blood was counted by flow ***,in vivo evidence about effects of Treg/th17 balance during liver injury was obtained in rat hepatitis and fibrosis ***:We observed AHB patients’peripheral th17 cell increased significantly while HBV-LF patients were conducive to Treg ***17/Treg ratio increased in AHB an

关键词： th17cells Treg cells Hepatitis B Fibrosis

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TLR4-MyD88 pathway and th1/th17 cells are required for the development of polymyositis

TLR4-MyD88 pathway and Th1/Th17 cells are required for the d...

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第十届全国免疫学学术大会

作者： Hongya Zhang Fangyuan He Juan Kang Ming Shi Gang Zhao Hongge Jia Xijing Hospital Fourth Military Medical University

BACKGROUND:Polymyositis(PM)is a kind of autoimmune diseases,causing severe muscle disorders but still lacks effective *** studies have showed that toll-like receptor 4(TLR4)is one of key players in the process of autoimmune ***,we still lack the knowledge about whether TLR4 is involved in PM pathology as ***:Here we demonstrated a possible involvement of TLR4 and its downstream effectors(*** D88 and NF-κB)in an experimental autoimmune myositis(EAM)mouse model and 22 PM patients using RT-PCR,IHC,***:Immunostaining and RT-PCR results showed that the expression of TLR4,My D88,and NF-κB was significantly upregulated in the muscle tissues in either EAM model or 22 patients with *** chip assay showed an increased levels of various pro-inflammatory cytokines,such as IL-1β,IL-6,IL-10,IL-12,TNF-α,and TGF-βin the serum of EAM ***,m RNA expression levels of T-bet and RORγt,two essential transcription factors for th1 and th17 cell differentiation respectively,were significantly increased in PM patients and EAM ***,levels of IFN-γand IL-17 secreted by th1 and th17 cells respectively were elevated as ***,all the factors above were reduced in the spleen of EAM *** analysis revealed that the expression levels of these factors were positively correlated with the degree of muscle inflammation in EAM ***:Our present study provided the first evidence that TLR4-My D88 pathway and th1/th17 cells may play important roles in the development of PM.

关键词： Toll-like receptor 4 Myeloid differentiation factor 88 Nuclear Factor-kappaB th1 cells th17cells

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MicroRNA-125b regulates th17/Treg cell differentiation and is associated with juvenile idiopathic arthritis

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World Journal of Pediatrics 2020年第1期16卷 99-110页

作者： Zhi-Dan Fan Qian Cao Na Huang Le Ma Hui-Hui Ma Ya-Yuan Zhang Hai-Guo Yu Guo-Ping Zhou Department of Pediatrics The First Affiliated Hospital of Nanjing Medical UniversityNanjing 210029China Department of Rheumatology and Immunology Children's Hospital of Nanjing Medical UniversityNanjing 210008China

Background Juvenile idiopathic arthritis(JIA)is the most common rheumatic disease in childhood driven by aberrant pathways of T-cell activation.T helper 17(th17)/regulatory T cell(Treg)imbalance plays critical roles in the pathogenesis of ***-125b(miR-125b)was upregulated after the activation of the initial CD4^+T cells,and could regulate the differentiation of CD4^+T ***,the effects of miR-125b on th17/Treg imbalance and differentiation of th 17/Treg cells remain *** In this study,we evaluated the expression of miR-125b in the peripheral blood mononuclear cells(PBMCs)of children with JIA,and the relationship of miR-125b with th17/Treg ***,we used lentivirus vector-mediated overexpression technology to investigate the regulatory function of miR-125b in CD4^+T cells or dendritic cell/CD4^+T co-culture *** Decreased miR-125b expression in PBMCs and CD4^+T cells of JIA patients was negatively correlated with the ratio of th17/Treg *** also correlated negatively with retinoic acid receptor-related orphan receptorγt but positively with Forkhead box protein 3 at transcriptional ***,we found that miR-125b overexpression inhibited th17 cell differentiation,whereas facilitated the differentiation of Treg ***-125b upregulation led to the decrease of th 17-secreting cytokines but the increase of the Treg-secreting *** Our results demonstrate that miR-125b participated in regulating thl7/Treg cell differentiation and imbalance in JIA *** findings provide novel insight into the critical role of miR-125b in the th17/Treg imbalance of JIA,and raise the distinct possibility that miR-125b may prove to be a potential therapeutic target for JIA.

关键词： CD4^+T-cell differentiation Juvenile idiopathic arthritis MicroRNA-125b th17cells Treg cells

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