传出细胞增多
巨噬细胞
炎症
吞噬作用
调节器
表型
促炎细胞因子
细胞生物学
生物
免疫学
肝损伤
体外
遗传学
基因
药理学
作者
Lara Campana,Philip Lewis,Antonella Pellicoro,Rebecca L. Aucott,Janet Tak Yun Man,Eoghan O’Duibhir,Sarah Mok,Sofía Ferreira-González,Eilidh Livingstone,Stephen N. Greenhalgh,Katherine L. Hull,Timothy J. Kendall,Douglas Vernimmen,Neil C. Henderson,Luke Boulter,Christopher D. Gregory,Yi Feng,Stephen M. Anderton,Stuart J. Forbes,John P. Iredale
出处
期刊:Journal of Immunology
[The American Association of Immunologists]
日期:2018-02-01
卷期号:200 (3): 1169-1187
被引量:72
标识
DOI:10.4049/jimmunol.1701247
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 proinflammatory to restorative. Using sterile liver injury models, we show that the STAT3-IL-10-IL-6 axis is a positive regulator of macrophage efferocytosis, survival, and phenotypic conversion, directly linking debris engulfment to tissue repair.
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