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Transforming growth factor-beta inhibits coxsackievirus-mediated autoimmune myocarditis

Marc S Horwitz1, Maria Knudsen, Alex Ilic

  • 1Microbiology and Immunology, University of British Columbia, Vancouver, BC, Canada. mhorwitz@interchange.ubc.ca

Viral Immunology
|January 5, 2007
PubMed

Insights

Transforming growth factor-beta (TGF-beta) in pancreatic beta cells prevents autoimmune myocarditis after coxsackie B virus (CBV) infection. TGF-beta reduces viral replication and controls CBV-mediated heart autoimmunity.

Area of Science:

  • Immunology
  • Virology
  • Cardiology

Background:

  • Clinical myocarditis precedes dilated cardiomyopathy and heart failure.
  • Coxsackie B virus (CBV) causes nearly 30% of recent myocarditis cases.
  • CBV infection leads to chronic autoimmunity originating in the pancreas.

Purpose of the Study:

  • To investigate if immunosuppressive cytokines limit heart autoimmunity.
  • To determine the efficacy of pancreatic cytokine expression in preventing CBV-induced myocarditis.

Main Methods:

  • Transgenic mice expressing cytokines (transforming growth factor-beta (1) [TGF-beta] or interleukin-4) in pancreatic beta cells were infected with CBV.
  • Immune responses and viral load in the pancreas and heart were assessed.

Main Results:

  • Transgenic TGF-beta expression in pancreatic beta cells prevented autoimmune myocarditis post-CBV infection.
  • Interleukin-4 expression did not inhibit CBV-mediated heart disease.
  • TGF-beta reduced viral replication and increased macrophage recruitment in the pancreas.

Conclusions:

  • Pancreatic TGF-beta expression is protective against CBV-induced autoimmune myocarditis.
  • TGF-beta effectively controls both viral replication and autoimmunity.
  • Targeting pancreatic TGF-beta may offer a therapeutic strategy for myocarditis and heart failure.

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