调节性B细胞
单核细胞
CCR2型
医学
心肌梗塞
内科学
促炎细胞因子
白细胞介素10
趋化因子
心室重构
炎症
免疫学
免疫系统
趋化因子受体
作者
Jiao Jiao,Shujie He,Yiqiu Wang,Yang Lu,Muyang Gu,Dan Li,Tingting Tang,Shaofang Nie,Min Zhang,Bingjie Lv,Jingyong Li,Ni Xia,Xiang Cheng
标识
DOI:10.1007/s00395-021-00886-4
摘要
Overactivated inflammatory responses contribute to adverse ventricular remodeling after myocardial infarction (MI). Regulatory B cells (Bregs) are a newly discovered subset of B cells with immunomodulatory roles in many immune and inflammation-related diseases. Our study aims to determine whether the expansion of Bregs exerts a beneficial effect on ventricular remodeling and explore the mechanisms involved. Here, we showed that adoptive transfer of Bregs ameliorated ventricular remodeling in a murine MI model, as demonstrated by improved cardiac function, decreased scar size and attenuated interstitial fibrosis without changing the survival rate. Reduced Ly6Chi monocyte infiltration was found in the hearts of the Breg-transferred mice, while the infiltration of Ly6Clo monocytes was not affected. In addition, the replenishment of Bregs had no effect on the myocardial accumulation of T cells or neutrophils. Mechanistically, Bregs reduced the expression of C-C motif chemokine receptor 2 (CCR2) in monocytes, which inhibited proinflammatory monocyte recruitment to the heart from the peripheral blood and mobilization from the bone marrow. Breg-mediated protection against MI was abrogated by treatment with an interleukin 10 (IL-10) antibody. Finally, IL-10 neutralization reversed the effect of Bregs on monocyte migration and CCR2 expression. The present study suggests a therapeutic value of Bregs in limiting ventricular remodeling after MI through decreasing CCR2-mediated monocyte recruitment and mobilization.
科研通智能强力驱动
Strongly Powered by AbleSci AI