中国免疫学杂志2024，Vol.40Issue(9)：1808-1814,7.DOI:10.3969/j.issn.1000-484X.2024.09.003
乙型肝炎病毒抑制M1巨噬细胞TLR4、NLRP3及下游因子促进免疫逃逸
Hepatitis B virus inhibits TLR4,NLRP3 and downstream factors of M1 macrophages to promote immune escape
摘要
Abstract
Objective:To explore the mechanism of hepatitis B virus(HBV)inhibiting M1 macrophages to promote immune escape,and to provide targets and strategies for antiviral therapy.Methods:The human monocyte cell line THP-1 was induced into M1 macrophages with PMA+LPS+IFN-γ.Cell morphological changes and the expressions of CD68,CD86,HLA-DR and functional molecules IL-1β,IL-6,TNF-α in M1 macrophages were detected by flow cytometry and RT-qPCR to identify M1 macrophages.HBV stable replication cell line HepG2.2.15 were co-cultured with M1 macrophages,and the expression of HBV-DNA was detected by qP-CR.The expression of CD68,CD86 and HLA-DR were detected by flow cytometry.The expressions of functional molecules TLR4,NLRP3,Caspase-1,pro-caspase-1,caspase-1 p20,IL-1β and IL-18 in M1 macrophages were determined by RT-qPCR and Western blot.Apoptosis rate was detected by flow cytometry,and the expression of apoptosis related protein cleaved-caspase-3 was determined by Western blot.Results:THP-1 was successfully induced to differentiate into M1 macrophages.M1 macrophages inhibited HBV repli-cation(P<0.05).HBV inhibited the expressions of CD68,CD86 and HLA-DR in M1 macrophages(P<0.01).HBV inhibited the ex-pressions of TLR4,NLRP3,Caspase-1,caspase-1 p20,IL-1β and IL-18 in M1 macrophages(P<0.01).HBV induced M1 macro-phage apoptosis(P<0.05).Conclusion:HBV inhibits M1 macrophages and their functional molecules TLR4,NLRP3 and down-stream factors,reduces the synthesis and secretion of inflammatory factors,induces apoptosis,and then promotes immune escape,re-sulting in the persistence and replication of HBV in the body.关键词
HBV/TLR4/NLRP3/M1巨噬细胞/免疫逃逸Key words
HBV/TLR4/NLRP3/M1 macrophages/Immune escape分类
基础医学引用本文复制引用
张自力,刘佳敏,曾蓉,余玲,叶青,徐旭,潘万龙..乙型肝炎病毒抑制M1巨噬细胞TLR4、NLRP3及下游因子促进免疫逃逸[J].中国免疫学杂志,2024,40(9):1808-1814,7.基金项目
国家自然科学基金预研项目(CBY19-YZ07) （CBY19-YZ07）
南充市市校科技战略合作专项(22SXQT0318). （22SXQT0318）
