J Clin Invest. 2021 Jul 1;131(13). doi: 10.1172/JCI150555.
The biphasic wound-healing response in the heart after myocardial infarction involves an initial inflammatory phase followed by a more prolonged period of inflammation resolution, tissue repair, and scar formation. Infiltrating proinflammatory Ly6Chi monocytes and monocyte-derived macrophages are key drivers of the inflammatory phase and are also the source of the locally generated reparative macrophages that promote inflammation resolution. In this issue of the JCI, Sicklinger et al. from the Leuschner laboratory uncover a salutary role for cardiac basophils in this process. The authors demonstrated that basophils promote healing and proper scar formation and also limit late cardiac remodeling by augmenting reparative macrophages in the infarcted heart, in part via basophil-derived enhancement of cardiac IL-4 and IL-13 levels. These findings underscore the potentially disproportionate (relative to cell numbers) yet essential biological effects of immune cells of low abundance on cardiac repair and remodeling, related in part to amplification of downstream macrophage responses via secreted cytokines.
心肌梗死后心脏的双相愈合反应包括初始炎症阶段，随后是更持久的炎症消退、组织修复和瘢痕形成。浸润的促炎 Ly6Chi 单核细胞和单核细胞衍生的巨噬细胞是炎症阶段的关键驱动因素，也是局部产生促进炎症消退的修复性巨噬细胞的来源。在本期 JCI 中，Leuschner 实验室的 Sicklinger 等人揭示了心脏嗜碱性粒细胞在这一过程中的有益作用。作者证明，嗜碱性粒细胞通过增强梗死心脏中的修复性巨噬细胞来促进愈合和适当的瘢痕形成，并限制晚期心脏重塑，部分是通过嗜碱性粒细胞衍生的心脏 IL-4 和 IL-13 水平增强。这些发现强调了低丰度免疫细胞对心脏修复和重塑的潜在不成比例（相对于细胞数量）但至关重要的生物学影响，部分原因是通过分泌细胞因子放大下游巨噬细胞反应。
