The transition from viral to autoimmune myocarditis

Susan L. Hill, Noel R. Rose

Research output: Contribution to journalArticle

Abstract

Myocarditis offers a unique opportunity to study the factors contributing to its transition from a viral infection to an autoimmune disease. In this article, we review recent studies on the role of nitric oxide (NO), gamma interferon (IFN-γ) and interleukin 12 (IL-12) in the progression from early (viral) to late (autoimmune) phases of myocarditis induced by Coxsackievirus B3 (CB3) in highly susceptible (A.CA) and moderately susceptible (B10.M) mice. NO plays a paradoxical role, being protective in early stages but detrimental later in the course of disease. Treatment with antibody to IFN-γ reduced early disease, but had little effect on the severity of cardiac lesions at later times. Treatment with recombinant (r) IL-12 significantly reduced the autoimmune cardiac lesions in moderately susceptible B10.M mice, but had no measurable effect in highly susceptible A.CA animals. These studies provide evidence that the profile of inflammatory mediators produced early in the course of viral infection determines the later development of autoimmune disease.

Original languageEnglish (US)
Pages (from-to)169-176
Number of pages8
JournalAutoimmunity
Volume34
Issue number3
DOIs
StatePublished - Jan 1 2001

Keywords

  • Cardiac myosin
  • Coxsackievirus
  • IFN-γ
  • IL-12
  • Myocarditis
  • Nitric oxide

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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