Stress granule assembly impairs macrophage efferocytosis to aggravate allergic rhinitis in mice

Ye Zhou, Zixuan Yang, Yuanyuan Wang, Yue Dong, Tianyu Wang, Yunhui Li, Caiquan Liang, Yanfang Liu, Zhixuan Li, Shanrong Liu, Liangchen Gui, Yiwen Fan, Ting Lei, Kaiwei Jia, Liyuan Zhang, Mu Wang, Wen Nie, Long Chen, Mingrui Ma, Yanfeng Wu, Cuiping Zhong, Huanhai Liu and Jin Hou ()
Additional contact information
Ye Zhou: Second Military Medical University
Zixuan Yang: Second Affiliated Hospital of Second Military Medical University
Yuanyuan Wang: Second Military Medical University
Yue Dong: Second Military Medical University
Tianyu Wang: Second Affiliated Hospital of Second Military Medical University
Yunhui Li: Second Military Medical University
Caiquan Liang: Second Affiliated Hospital of Second Military Medical University
Yanfang Liu: Second Military Medical University
Zhixuan Li: Second Military Medical University
Shanrong Liu: Second Military Medical University
Liangchen Gui: Second Military Medical University
Yiwen Fan: Second Military Medical University
Ting Lei: Second Military Medical University
Kaiwei Jia: Second Military Medical University
Liyuan Zhang: Second Military Medical University
Mu Wang: Second Military Medical University
Wen Nie: Second Military Medical University
Long Chen: Second Military Medical University
Mingrui Ma: Second Military Medical University
Yanfeng Wu: Second Military Medical University
Cuiping Zhong: No. 940 Hospital of Joint Logistics Support Force of People’s Liberation Army
Huanhai Liu: Second Affiliated Hospital of Second Military Medical University
Jin Hou: Second Military Medical University

Nature Communications, 2025, vol. 16, issue 1, 1-18

Abstract: Abstract Cytoplasmic stress granules (SG) assemble in response to stress-induced translational arrest and are key signaling hubs orchestrating cell fate and regulating various physiological and pathological processes. However, the role of SG formation in the progression of allergic diseases is incompletely understood. Here, by analyzing the nasal tissues of allergic rhinitis (AR) mouse models and AR patients, we find that SGs assemble specifically in the macrophages within the nasal mucosa and promote AR progression by restraining the efferocytotic ability of macrophages, ultimately resulting in reduced Mres generation and IL-10 production. Mechanistically, intracellular m7G-modified Lrp1 mRNA, encoding for a typical efferocytosis receptor, is transported by the m7G reader QKI7 into stress-induced SGs, where Lrp1 mRNA is sequestered away from the translation machinery, ultimately resulting in reduced macrophage efferocytosis. Therefore, SG assembly impairs macrophage efferocytosis and aggravates AR, and the inhibition of SGs bears considerable potential in the targeted therapy.

Date: 2025
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DOI: 10.1038/s41467-025-60920-0

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