免疫学
实验性自身免疫性脑脊髓炎
免疫系统
生物
自身免疫
细胞因子
自身免疫性疾病
系统性红斑狼疮
细胞生物学
疾病
抗体
医学
内科学
作者
Yingying Cai,Cuixia Yang,Xiaohan Yu,Jie Qian,Min Dai,Yan Wang,Chaoyan Qin,Weiming Lai,Shuai Chen,Tingting Wang,Jinfeng Zhou,Ningjia Ma,Yue Zhang,Ru Zhang,Nan Shen,Xin Xie,Changsheng Du
出处
期刊:Journal of Immunology
[The American Association of Immunologists]
日期:2018-12-12
卷期号:202 (2): 407-420
被引量:8
标识
DOI:10.4049/jimmunol.1800261
摘要
Abstract Altered migration and immune responses of dendritic cells (DCs) lead to inflammatory and autoimmune diseases. Our studies demonstrated that β-arrestin 2 deficiency promoted migration and cytokine production of mouse bone marrow–derived DCs. We further found that β-arrestin 2 directly interacted with Zbtb46, a DC-specific transcription factor. What’s more, our results suggested that the interaction between β-arrestin 2 and Zbtb46 might negatively regulate DC migration. Using RNA sequencing, we indicated that genes CD74, NR4A1, and ZFP36 might be the target genes regulated by the interaction between β-arrestin 2 and Zbtb46. Mice with selective deficiency of β-arrestin 2 in DCs developed severer experimental autoimmune encephalomyelitis with more DC infiltration in the CNS and increased IL-6 in serum. In the systemic lupus erythematosus mice model, Arrb2fl/fl Itgax-cre+ mice were prone to exacerbation of lupus nephritis with a higher level of IL-6 and DC accumulation. Taken together, our study identified β-arrestin 2 as a new regulator of DC migration and immune properties, providing new insights into the mechanisms underlying the development of autoimmune disease.
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