Department of Medicine, Columbia University, New York, NY 10032, USA.
Department of Medicine, Columbia University, New York, NY 10032, USA; Department of Biochemistry, Marmara University, Istanbul, Turkey.
Immunity. 2018 Oct 16;49(4):666-677.e6. doi: 10.1016/j.immuni.2018.07.015. Epub 2018 Oct 2.
Regulatory T (Treg) cell responses and apoptotic cell clearance (efferocytosis) represent critical arms of the inflammation resolution response. We sought to determine whether these processes might be linked through Treg-cell-mediated enhancement of efferocytosis. In zymosan-induced peritonitis and lipopolysaccharide-induced lung injury, Treg cells increased early in resolution, and Treg cell depletion decreased efferocytosis. In advanced atherosclerosis, where defective efferocytosis drives disease progression, Treg cell expansion improved efferocytosis. Mechanistic studies revealed the following sequence: (1) Treg cells secreted interleukin-13 (IL-13), which stimulated IL-10 production in macrophages; (2) autocrine-paracrine signaling by IL-10 induced Vav1 in macrophages; and (3) Vav1 activated Rac1 to promote apoptotic cell engulfment. In summary, Treg cells promote macrophage efferocytosis during inflammation resolution via a transcellular signaling pathway that enhances apoptotic cell internalization. These findings suggest an expanded role of Treg cells in inflammation resolution and provide a mechanistic basis for Treg-cell-enhancement strategies for non-resolving inflammatory diseases.
调节性 T(Treg)细胞反应和凋亡细胞清除(吞噬作用)是炎症消退反应的关键环节。我们试图确定这些过程是否可能通过 Treg 细胞介导的吞噬作用增强而相关。在酵母聚糖诱导的腹膜炎和脂多糖诱导的肺损伤中,Treg 细胞在消退早期增加,而 Treg 细胞耗竭则降低了吞噬作用。在晚期动脉粥样硬化中,由于吞噬作用缺陷驱动疾病进展,Treg 细胞的扩张改善了吞噬作用。机制研究揭示了以下顺序:(1)Treg 细胞分泌白细胞介素 13(IL-13),刺激巨噬细胞产生白细胞介素 10(IL-10);(2)IL-10 的自分泌-旁分泌信号诱导巨噬细胞中的 Vav1;(3)Vav1 激活 Rac1 以促进凋亡细胞的吞噬。总之,Treg 细胞通过增强凋亡细胞内化的细胞间信号通路,在炎症消退过程中促进巨噬细胞的吞噬作用。这些发现表明 Treg 细胞在炎症消退中具有扩展的作用,并为非解决性炎症性疾病的 Treg 细胞增强策略提供了机制基础。