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Updated: Jan 14, 2026

A High Resolution Method to Monitor Phosphorylation-dependent Activation of IRF3
Published on: January 24, 2016
ASFV activates STAT3 to induce proviral M2 macrophage polarization
Yanru Chen1, Haowei Chen1, Weijia Zhang1
1State Key Laboratory of Agricultural Microbiology, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan, China; Key Laboratory of Preventive Veterinary Medicine in Hubei Province, The Cooperative Innovation Center for Sustainable Pig Production, Wuhan, China; Key Laboratory of Development of Veterinary Diagnostic Products, Ministry of Agriculture of the People's Republic of China, Wuhan, China; International Research Center for Animal Disease, Ministry of Science and Technology of the People's Republic of China, Wuhan, China; Hubei Jiangxia Laboratory, Wuhan, China.
African swine fever virus (ASFV) promotes M2 macrophage polarization via STAT3, impairing immune responses. Inhibiting STAT3 reduces ASFV replication and restores immune cell function, offering therapeutic insights.
Area of Science:
- Veterinary Virology
- Immunology
- Cell Biology
Background:
- African swine fever (ASF) is a highly infectious viral disease impacting the global pig industry.
- Macrophages are key targets of the African swine fever virus (ASFV), but their polarization during infection is unclear.
Purpose of the Study:
- To investigate macrophage phenotypic changes during ASFV infection.
- To elucidate the role of STAT3 in ASFV-induced macrophage polarization.
- To assess the impact of M2 polarization on viral replication and adaptive immunity.
Main Methods:
- Observation of peripheral blood monocytes in ASFV-infected pigs.
- In vitro macrophage polarization assays.
- STAT3 inhibition using STATTIC.
- Co-culture experiments with T cells (MLR system).
Main Results:
- ASFV infection increased M2 monocyte populations.
- ASFV induced M2 polarization via STAT3 phosphorylation.
- STAT3 inhibition blocked M2 polarization and suppressed ASFV replication.
- M2 macrophages showed reduced killing capacity and impaired T cell activation.
Conclusions:
- ASFV manipulates macrophage polarization to M2 phenotype through STAT3 signaling.
- M2 macrophages contribute to ASFV immune evasion and persistence.
- Targeting STAT3 may be a viable strategy for ASF control.
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