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CARD9 orchestrates tissue damage in APAP-induced hepatitis via TREM2-mediated sensing cell death
Zaopeng Yang1,2,3, Shiqi Li1, Renlin Lu1
1Institute for Immunology and School of Basic Medical Sciences, Tsinghua University, Beijing, 100084, China.
Journal of Immunology (Baltimore, Md. : 1950)
|January 27, 2026
Summary
Cardiotomy-induced gene 9 (CARD9) in Kupffer cells worsens acetaminophen-induced liver injury by increasing inflammation. TREM2 receptors on Kupffer cells recognize cell death components, driving sterile inflammation.
Area of Science:
- Immunology
- Hepatology
- Molecular Biology
Background:
- Acetaminophen (N-acetyl-para-aminophenol [APAP])-induced liver injury involves innate immune responses and tissue damage.
- The precise mechanisms of sterile hepatitis are not fully understood.
- Cardiotomy-induced gene 9 (CARD9) regulates NF-κB activation in anti-pathogen immunity but its role in sterile liver injury is unknown.
Purpose of the Study:
- To investigate the role of CARD9 in acetaminophen-induced liver injury.
- To elucidate the cellular and molecular mechanisms of sterile inflammation in the liver.
Main Methods:
- Utilized a mouse model of acetaminophen-induced liver injury.
- Analyzed CARD9 expression in Kupffer cells.
- Investigated TREM2 receptor function in Kupffer cells.
Main Results:
- CARD9 expression in Kupffer cells exacerbates liver damage.
- CARD9 amplifies the production of pro-inflammatory factors in sterile hepatitis.
- TREM2 receptors on Kupffer cells recognize damage-associated molecular patterns (DAMPs) released from dying hepatocytes.
- TREM2 acts as an upstream signaling receptor orchestrating sterile inflammation.
Conclusions:
- CARD9 plays a detrimental role in acetaminophen-induced liver injury by promoting inflammation.
- TREM2 signaling in Kupffer cells is critical for recognizing cell death and driving sterile liver inflammation.
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