MBD2通路在重症哮喘中作用的研究进展  

Progress on the role of MBD2 pathway in severe asthma

作　　者：吴定将 张秀峰 WU Dingjiang;ZHANG Xiufeng(Department of Respiratory Medicine,the Second Affiliated Hospital of Hainan Medical University,Haikou 570216,China)

机构地区：[1]海南医学院第二附属医院呼吸内科,海南海口570216

出　　处：《基础医学与临床》2024年第8期1165-1169,共5页Basic and Clinical Medicine

基　　金：国家自然科学基金(81960006)。

摘　　要：重症哮喘是一种对糖皮质激素治疗不敏感的慢性炎性疾病。在重症哮喘的发病过程中,辅助性T细胞17(Th17)及白细胞介素17(IL-17)起着重要的作用,主要是通过以聚集中性粒细胞浸润来加重哮喘的严重程度。甲基-CpG结合域蛋白2(MBD2)在Th17细胞由初始CD4+T细胞分化而来的过程中起着重要作用,能正向调控Th17分化和IL-17表达。MBD2与干扰素调节因子4(IRF4)、细胞因子信号转导抑制蛋白3(SOCS3)、低氧诱导因子-1α(HIF-1α)及畸胎样激酶1(MINK1)启动子区的CpG岛结合,进而可导致甲基化,调节Th17细胞分化,并参与严重哮喘的发病机制。Severe asthma is a chronic inflammatory disease that is not sensitive to glucocorticoid treatment.In the pathogenesis of severe asthma,T helper cell 17(Th17)and interleukin 17(IL-17)play an important role,mainly by aggregating the infiltration of neutrophil to aggravate the severity of asthma.Methyl-CpG-binding protein 2(MBD2)plays an important role in the differentiation of Th17 cells from naive CD4+T cells,positively regulate Th17 differentiation and IL-17 expression.MBD2 binds to the CpG islands in the promoter region of interferon regulatory factor 4(IRF4),suppressor of cytokine signaling 3(SOCS3),hypoxia-inducible factor-1α(HIF-1α)and misshapen like kinase 1(MINK1),which leads to methylation,regulates the differentiation of Th17 cells,and participates in the pathogenesis of severe asthma.

关 键 词：重症哮喘 甲基-CpG结合域蛋白2(MBD2) 辅助性T细胞17 

分 类 号：R562[医药卫生—呼吸系统]