ITP发病机制研究进展  

Progress in the pathogenesis of ITP

作　　者：盘冬兰 陆盅伃[1] Pan DongLan;Lu Zhongyu(Maternity and Child Care Intensive Medicine Guangxi Zhuang Autonomous Region,Nanning Guangxi,530000,China)

机构地区：[1]广西壮族自治区妇幼保健院重症医学科,广西南宁530000

出　　处：《医药前沿》2020年第5期6-7,共2页Journal of Frontiers of Medicine

摘　　要：特发性血小板减少性紫癜(Idiopathic thrombocytopenic purpura,ITP)属于自身免疫性疾病,又称为特发性血小板减少性紫癜。机体内发生的免疫反应可对血小板造成破坏,另外,还对巨噬细胞和血小板的成熟具有重要影响。ITP发病机制复杂,目前认为与血小板、巨噬细胞发生的异常凋亡有关,主要受机体内调节性B细胞异常、细胞因子异常、T细胞比例异常及DNA甲基化、微小RNA异常的作用。本文从ITP发病机制的不同方面进行综述,为ITP的治疗提供依据。Idiopathic thrombocytopenic purpura(ITP)is an autoimmune disease,also known as idiopathic thrombocytopenic purpura.The immune response that occurs in the body can cause damage to platelets,in addition,it has an important effect on the maturation of macrophages and platelets.The pathogenesis of ITP is complex.It is thought to be related to abnormal apoptosis of platelets and macrophages.It is mainly regulated by regulatory B cell abnormalities,abnormal cytokines,abnormal T cell ratio,DNA methylation and microRNA abnormalities.This study will systematically review different aspects of the pathogenesis of ITP and provide a basis for the treatment of ITP.

关 键 词：免疫性血小板减少性紫癜 B细胞 T细胞 DNA甲基化 微小RNA 

分 类 号：R593.3[医药卫生—内科学]