Epigenetic regulation in B-cell maturation and its dysregulation in autoimmunity  

作　　者：Haijing Wu Yaxiong Deng Yu Feng Di Long Kongyang Ma Xiaohui Wang Ming Zhao Liwei Lu Qianjin Lu 

机构地区：[1]Department of Dermatology,Second Xiangya Hospital,Central South University,Hunan Key Laboratory of Medical Epigenomics,Changsha,Hunan 410011,China [2]Department of Pathology and Shenzhen Institute of Research and Innovation,The University of Hong Kong,Hong Kong,China

出　　处：《Cellular & Molecular Immunology》2018年第7期676-684,共9页中国免疫学杂志（英文版）

基　　金：This work was supported by the National Natural Science Foundation of China(Nos.81220108017,81522038,81602767,81430074,91442116,81373195 and 81771761);National Basic Research Program of China(No.2014CB541904);the Programs of Science-Technology Commission of Hunan Province(2013F J4202);the Natural Science Foundation of Hunan Province(2017JJ3453);the Natural Key Clinical Speciality Construction Project of National Health and Family Planning Commission of the People’s Republic of China.

摘　　要：B cells have a critical role in the initiation and acceleration of autoimmune diseases, especially those mediated byautoantibodies. In the peripheral lymphoid system, mature B cells are activated by self or/and foreign antigens andsignals from helper T cells for differentiating into either memory B cells or antibody-producing plasma cells.Accumulating evidence has shown that epigenetic regulations modulate somatic hypermutation and class switchDNA recombination during B-cell activation and differentiation. Any abnormalities in these complex regulatoryprocesses may contribute to aberrant antibody production, resulting in autoimmune pathogenesis such as systemiclupus erythematosus. Newly generated knowledge from advanced modern technologies such as next-generationsequencing, single-cell sequencing and DNA methylation sequencing has enabled us to better understand B-cellbiology and its role in autoimmune development. Thus this review aims to summarize current research progress inepigenetic modifications contributing to B-cell activation and differentiation, especially under autoimmuneconditions such as lupus, rheumatoid arthritis and type 1 diabetes.

关 键 词：AUTOIMMUNITY B cell DNA methylation histone modification MICRORNA 

分 类 号：R73[医药卫生—肿瘤]