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IL-19 Modulates Antiviral Immunity and Inflammation via IL-20RB/STAT3/TRIM22 Signaling Pathway
Xinyu Zhang1,2, Fan Wu1,2, Xinru Hu1,2
1School of Public Health (Shenzhen), Sun Yat-Sen University, Shenzhen, China.
Journal of Medical Virology
|July 20, 2026
Summary
Interleukin-19 (IL-19) exhibits antiviral properties by activating the IL-20RB/STAT3 pathway, enhancing interferon-lambda (IFN-λ) secretion to suppress viral replication. However, IL-19 also exacerbates inflammation, highlighting its dual role in immune responses.
Area of Science:
- Immunology
- Virology
- Molecular Biology
Background:
- Interleukins (ILs) are key immune signaling molecules with potential for antiviral therapies.
- Interleukin-19 (IL-19) is upregulated during viral infections, but its specific role remains unclear.
Purpose of the Study:
- To investigate the antiviral activity and underlying mechanisms of IL-19.
- To elucidate the dual role of IL-19 in viral infections and inflammation.
Main Methods:
- Investigated IL-19 signaling pathway involving IL-20RB and STAT3.
- Assessed the impact of IL-19 on TRIM22 expression and IFN-λ secretion.
- Evaluated viral replication and survival in murine models of HSV-1 infection.
Main Results:
- IL-19 activates the IL-20RB/STAT3 pathway, inducing TRIM22 and enhancing IFN-λ secretion.
- IL-19 significantly reduced HSV-1 replication in mouse brain and lung tissues.
- IL-19 administration led to aggravated pulmonary inflammation and did not improve survival.
Conclusions:
- IL-19 possesses direct antiviral effects by modulating the IL-20RB/STAT3/TRIM22/IFN-λ axis.
- IL-19 acts as a dual-function cytokine, exhibiting both antiviral and pro-inflammatory properties.
- The immunomodulatory functions of cytokines are complex and context-dependent during viral infections.
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