B细胞激活因子在免疫性血小板减少症发病机制中的研究现状  

Research status on B-cell-activating factor in pathogenesis of immune thrombocytopenia

作　　者：李会婷 王丹丹[1] 敖慧娟 毕慧[1] Li Huiting;Wang Dandan;Ao Huijuan;Bi Hui(Second Affiliated Hospital of Kunming Medical University,Kunming 650106,Yunnan Province,China)

机构地区：[1]昆明医科大学第二附属医院,昆明650106

出　　处：《国际输血及血液学杂志》2023年第1期19-25,共7页International Journal of Blood Transfusion and Hematology

基　　金：云南省科技厅-昆医联合专项(2018FE001-049);昆明医科大学研究生创新基金(2022S267)。

摘　　要：免疫性血小板减少症(ITP)是一种自身免疫性出血性疾病,B细胞参与抗体介导的血小板破坏被认为是ITP的病理生理学核心,因此以利妥昔单抗为代表的抗B细胞治疗成为ITP的主要治疗方法之一。B细胞激活因子(BAFF)是一种调控B细胞存活、分化的关键细胞因子,越来越多的证据显示BAFF与ITP发病存在联系。笔者拟就BAFF的生物学特点,BAFF与自身免疫、ITP的关系,以及BAFF调节在ITP中的作用等方面进行阐述,旨在BAFF抑制在ITP管理中的可行性。Immune thrombocytopenia(ITP)is an autoimmune hemorrhagic disease.Antibody-mediated platelet destruction in which B cells participate is considered to be the core of ITP pathophysiology.Therefore,anti-B cell therapy represented by rituximab has become one of the main treatment methods for ITP.B-cell-activating factor(BAFF)is a key cytokine that regulates survival and differentiation of B cell.More and more evidences show that BAFF is related to the pathogenesis of ITP.This article describes the biological characteristics of BAFF,the relationship between BAFF and autoimmunity and ITP,as well as the role of BAFF regulation in ITP,aiming at the feasibility of BAFF inhibition in ITP management.

关 键 词：血小板减少 B细胞活化因子 受体 B细胞活化因子 发病机制 

分 类 号：R558.2[医药卫生—血液循环系统疾病]