再生(生物学)
肺
人口
肺炎
免疫系统
巨噬细胞
生物
病理
细胞生物学
免疫学
医学
内科学
体外
生物化学
环境卫生
作者
Cecilia Ruscitti,Joan Abinet,Pauline Maréchal,Margot Meunier,Constance De meeûs,Domien Vanneste,Pierre Janssen,Mickaël Dourcy,Marc Thiry,Fabrice Bureau,Christoph Schneider,Bénédicte Machiels,Andrés Hidalgo,Florent Ginhoux,Benjamin G Dewals,Julien Guiot,Florence Schleich,Mutien‐Marie Garigliany,Akeila Bellahcène,Coraline Radermecker,Thomas Marichal
出处
期刊:Science immunology
[American Association for the Advancement of Science (AAAS)]
日期:2024-08-02
卷期号:9 (98)
被引量:1
标识
DOI:10.1126/sciimmunol.ado1227
摘要
The lung is constantly exposed to airborne pathogens and particles that can cause alveolar damage. Hence, appropriate repair responses are essential for gas exchange and life. Here, we deciphered the spatiotemporal trajectory and function of an atypical population of macrophages after lung injury. Post–influenza A virus (IAV) infection, short-lived monocyte-derived Ly6G-expressing macrophages (Ly6G + Macs) were recruited to the alveoli of lung perilesional areas. Ly6G + Macs engulfed immune cells, exhibited a high metabolic potential, and clustered with alveolar type 2 epithelial cells (AT2s) in zones of active epithelial regeneration. Ly6G + Macs were partially dependent on granulocyte-macrophage colony-stimulating factor and interleukin-4 receptor signaling and were essential for AT2-dependent alveolar regeneration. Similar macrophages were recruited in other models of injury and in the airspaces of lungs from patients with suspected pneumonia. This study identifies perilesional alveolar Ly6G + Macs as a spatially restricted, short-lived macrophage subset promoting epithelial regeneration postinjury, thus representing an attractive therapeutic target for treating lung damage.
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