作者
Dai Dai,Shuangshuang Gu,Xiaxia Han,Huihua Ding,Yang Jiang,Xiao‐Ou Zhang,Chao Yao,Soon-Min Hong,Jinsong Zhang,Yiwei Shen,Guojun Hou,Bo Qu,Haibo Zhou,Yuting Qin,Yuke He,Jianyang Ma,Zhihua Yin,Zhizhong Ye,Jie Qian,Qian Jiang,Lihua Wu,Qiang Guo,Sheng Chen,Chuanxin Huang,Leah C. Kottyan,Matthew T. Weirauch,Carola G. Vinuesa,Nan Shen
摘要
Age-associated B cells (ABCs) accumulate during infection, aging, and autoimmunity, contributing to lupus pathogenesis. In this study, we screened for transcription factors driving ABC formation and found that zinc finger E-box binding homeobox 2 (ZEB2) is required for human and mouse ABC differentiation in vitro. ABCs are reduced in ZEB2 haploinsufficient individuals and in mice lacking Zeb2 in B cells. In mice with toll-like receptor 7 (TLR7)–driven lupus, ZEB2 is essential for ABC formation and autoimmune pathology. ZEB2 binds to +20-kb myocyte enhancer factor 2b ( Mef2b )’s intronic enhancer, repressing MEF2B-mediated germinal center B cell differentiation and promoting ABC formation. ZEB2 also targets genes important for ABC specification and function, including Itgax . ZEB2-driven ABC differentiation requires JAK-STAT (Janus kinase-signal transducer and activator of transcription), and treatment with JAK1/3 inhibitor reduces ABC accumulation in autoimmune mice and patients. Thus, ZEB2 emerges as a driver of B cell autoimmunity.