PROS1/AXL signaling protects mice from lethal influenza infection by inducing M2 macrophage polarization.

Wenbo Zhu, Shao Wang, Shuangquan Liu, Qiang Fu, Hongbo Zhang

Abstract read

In one paragraph

Article in Acta biochimica et biophysica Sinica, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

Authors and funding

5 authors.

Wenbo ZhuThe First Affiliated Hospital, Clinical Medical Research Center, Hengyang Medical School, University of South China, Hengyang 421001, China.

Shao WangInstitute of Animal Husbandry and Veterinary Medicine, Fujian Academy of Agriculture Science, Fuzhou 350013, China.

Shuangquan LiuThe First Affiliated Hospital, Clinical Laboratory, Hengyang Medical School, University of South China, Hengyang 421001, China.

Qiang FuThe First Affiliated Hospital, Department of Rheumatology and Immunology, Hengyang Medical School, University of South China, Hengyang 421001, China.

Hongbo ZhangDepartment of Pediatrics, University of Pittsburgh School of Medicine, Pittsburgh, PA 15224, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

AXL, a member of the TAM (Tyro3, AXL, and Mertk) subfamily of RTKs, is abundantly expressed in lung tissue and has been implicated in viral infections and lung injury. PROS1, one of the ligands known to activate AXL, functions as an immunomodulator in many diseases. However, the role of PROS1/AXL signaling in influenza A virus (IAV) infection and infection-induced lung injury is largely unknown. In this study, we find that the exogenous administration of PROS1 mitigates lung injury and protects mice from lethal infection by IAVs through the activation of AXL. PROS1 induces the phosphorylation of AXL, which in turn recruits Gab1 and p85, a regulatory subunit of PI3K, to form a complex that activates Gab1 and its downstream PI3K/AKT/mTOR in alveolar macrophages.

Indexed as

AXLinfluenza infectionmacrophagepolarizationPROS1

Identifiers

PMID41158072

DOI10.3724/abbs.2025169

PMCPMC13191473

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