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CARD9 mediates T cell inflammatory response in Coxsackievirus B3-induced acute myocarditis

Changchun Sun1, Xian Zhang2, Yi Yu1

  • 1Department of Cardiology, Xinhua Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai 200092, China.

Cardiovascular Pathology : the Official Journal of the Society for Cardiovascular Pathology
|August 11, 2020
PubMed

Insights

Caspase-associated recruitment domain 9 (CARD9) deficiency reduces cardiac inflammation in viral myocarditis. CARD9 knockout mice showed lower levels of key inflammatory cytokines, suggesting CARD9’s role in the immune response to Coxsackievirus B3.

Area of Science:

  • Immunology
  • Cardiovascular Biology
  • Virology

Background:

  • Cardiac inflammation is a key factor in Coxsackievirus B3 (CVB3)-induced myocarditis.
  • Caspase-associated recruitment domain 9 (CARD9) is an adaptor protein crucial for innate immune signaling.

Purpose of the Study:

  • To investigate the role of CARD9 in the immune response during acute viral myocarditis.

Main Methods:

  • Comparison of CARD9 knockout (CARD9-/-) mice and wild-type (C57BL/6) mice infected with CVB3.
  • Analysis of myocardial tissue and serum samples collected 7 days postinfection.

Main Results:

  • CARD9 knockout mice exhibited significantly reduced mRNA and protein levels of transforming growth factor-β (TGF-β), interleukin-17A (IL-17A), and B-cell CLL/lymphoma 10 (BCL-10) in the myocardium.
  • Lower pathological inflammation scores and reduced serum levels of cytokines including IL-6, IL-10, IFN-γ, TGF-β, and IL-17A were observed in CARD9-/- mice.
  • These findings indicate a significant reduction in viral myocarditis severity upon CARD9 deficiency.

Conclusions:

  • CARD9 plays a critical role in mediating the immune response to CVB3-induced viral myocarditis.
  • CARD9-dependent secretion of pro-inflammatory cytokines contributes to cardiac inflammation in this model.

Keywords:
CARD9Coxsackievirus B3acute viral myocarditisimmune responseinflammation

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