Mast cells and innate cytokines are associated with susceptibility to autoimmune heart disease following Coxsackievirus B3 infection

Delisa Fairweather, Sylvia Frisancho-Kiss, Shannon Gatewood, Dolores Njoku, Ronelle Steele, Masheka Barrett, Noel R. Rose

Research output: Contribution to journalArticlepeer-review

76 Scopus citations

Abstract

The development of autoimmune disease involves a combination of genetic and environmental factors. Many autoimmune diseases are believed to be triggered by viral infections. Since the early, natural immune response to infection can determine the later development of the adaptive immune response, innate immunity likely influences the progression from viral immunity to autoimmunity. To investigate the role of the innate immune response on susceptibility to autoimmune disease, we compared the early cytokine response of mice susceptible or resistant to the development of autoimmune heart disease following viral infection. We found that susceptible BALB/c mice produced elevated levels of TNF-α, IL-1β, and IL-4 within hours of Coxsackievirus B3 (CB3) infection. These cytokines are known to be critical for the development of autoimmune heart disease, and are also rapidly produced from activated mast cells (MC). Degranulating MC were observed as early as 6 h following CB3 infection in the heart, and significantly higher numbers of MC were found in the spleen of susceptible BALB/c mice at this time. Thus, susceptibility to autoimmune heart disease can be determined as early as 6 h following viral infection in susceptible strains of mice.

Original languageEnglish (US)
Pages (from-to)131-145
Number of pages15
JournalAutoimmunity
Volume37
Issue number2
DOIs
StatePublished - Mar 2004

Keywords

  • Autoimmune disease
  • Cytokines
  • Innate immunity
  • Myocarditis

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Fingerprint

Dive into the research topics of 'Mast cells and innate cytokines are associated with susceptibility to autoimmune heart disease following Coxsackievirus B3 infection'. Together they form a unique fingerprint.

Cite this