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Abstract：
Although chronic inflammation is a central feature of heart failure (HF), the immune cell profiles differ with different underlying causes. This suggests that for immunomodulatory therapy in HF to be successful, it needs to be tailored to the specific etiology. Here, the authors demonstrate that monocyte-derived C-C chemokine receptor 2 (CCR2)+ macrophages infiltrate the heart early during pressure overload in mice, and that blocking this response either pharmacologically or with antibody-mediated CCR2+ monocyte depletion alleviates late pathological left ventricular remodeling and dysfunction, T-cell expansion, and cardiac fibrosis. Hence, suppression of CCR2+ monocytes/macrophages may be an important immunomodulatory therapeutic target to ameliorate pressure-overload HF.
摘要：
尽管慢性炎症是心力衰竭（HF）的主要特征，免疫细胞谱因不同的根本原因而不同。这表明，对于HF的免疫调节治疗是成功的，它需要根据特定的病因进行调整。这里,作者证明单核细胞来源的C-C趋化因子受体2（CCR2）+巨噬细胞在小鼠压力超负荷的早期浸润心脏，通过药理学或抗体介导的CCR2+单核细胞耗竭阻断这种反应可缓解晚期病理性左心室重构和功能障碍，T细胞扩增,和心脏纤维化。因此，抑制CCR2+单核细胞/巨噬细胞可能是改善压力超负荷HF的重要免疫调节治疗靶点。
