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The STAT3-IL10-IL6 pathway is a novel regulator of macrophage efferocytosis and phenotypic conversion in sterile liver injury

机译:STAT3-IL10-IL6途径是无菌性肝损伤中巨噬细胞放血和表型转化的新型调节剂

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摘要

The disposal of apoptotic bodies by professional phagocytes is crucial to effective inflammation resolution. Our ability to improve the disposal of apoptotic bodies by professional phagocytes is impaired by a limited understanding of the molecular mechanisms that regulate the engulfment and digestion of the efferocytic cargo. Macrophages are professional phagocytes necessary for liver inflammation, fibrosis and resolution, switching their phenotype from pro-inflammatory to restorative. Using sterile liver injury models, we show that the STAT3-IL10-IL6 axis is a positive regulator of macrophage efferocytosis, survival and phenotypic conversion, directly linking debris engulfment to tissue repair.
机译:专业吞噬细胞处理凋亡小体对于有效解决炎症至关重要。我们对调节吞噬细胞吞噬和消化的分子机制的有限了解削弱了我们通过专业吞噬细胞改善凋亡小体处置的能力。巨噬细胞是肝炎,纤维化和消融所必需的专业吞噬细胞,可将其表型从促炎性转变为恢复性。使用无菌肝损伤模型,我们表明STAT3-IL10-IL6轴是巨噬细胞放血,生存和表型转化的正向调节剂,直接将碎片吞噬与组织修复联系起来。

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