The healing myocardium mobilizes a distinct B-cell subset through a CXCL13-CXCR5-dependent mechanism
收藏干细胞与再生医学数据中心2022-02-20 更新2024-03-06 收录
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Recent studies have revealed that B-cells can influence post-myocardial infarction (MI) inflammation and repair, but the mechanisms controlling their mobilization and in situ activity remain poorly understood. Herein, we sought to dissect the mechanisms underlying B-cell cardiotropism and assess the B-cell antigen specificity profile in an experimental model of MI. Our study reveals that B-cells that are not antigen-specifically expanded readily infiltrate the infarcted myocardium via the CXCL13-CXCR5 axis. The restricted distribution of CXCR5 among hB cells could offer a suitable opportunity to selectively target this leukocyte subset therapeutically while minimally interfering with other local or systemic immunological processes.
提供机构：
Helmholtz Institute for RNA-based Infection Research
创建时间：
2022-02-20
