炎症
渗透(HVAC)
中性粒细胞胞外陷阱
细胞外
生物
细胞生物学
免疫学
气道
医学
材料科学
复合材料
外科
作者
Zebing Rao,Shaorui Liu,Zhicheng Li,Qiuying Wang,Feng Gao,Peng Han,Deshan Ren,Yang Zang,Hui Li,Mingcai Li,Qi Hu,Danyang He,Heping Xu
标识
DOI:10.1016/j.immuni.2024.09.001
摘要
Group 2 innate lymphoid cells (ILC2s) play a crucial role in allergic diseases by coordinating a complex network of various effector cell lineages involved in type 2 inflammation. However, their function in regulating airway neutrophil infiltration, a deleterious symptom of severe asthma, remains unknown. Here, we observed ILC2-dependent neutrophil accumulation in the bronchoalveolar lavage fluid (BALF) of allergic mouse models. Chromatography followed by proteomics analysis identified the alarmin high mobility group box-1 (HMGB1) in the supernatant of lung ILC2s initiated neutrophil chemotaxis. Genetic perturbation of Hmgb1 in ILC2s reduced BALF neutrophil numbers and alleviated airway inflammation. HMGB1 was loaded onto the membrane of lipid droplets (LDs) released from activated lung ILC2s. Genetic inhibition of LD accumulation in ILC2s significantly decreased extracellular HMGB1 abundance and BALF neutrophil infiltration. These findings unveil a previously uncharacterized extracellular LD-mediated immune signaling delivery pathway by which ILC2s regulate airway neutrophil infiltration during allergic inflammation.
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