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Chronic immune reactivity against persisting microbial antigen in the vasculature exacerbates atherosclerotic lesion

Philippe Krebs1, Elke Scandella, Beatrice Bolinger

  • 1Research Department, Kantonsspital St Gallen, Rorschacherstrasse 95, CH-9007 St Gallen, Switzerland.

Arteriosclerosis, Thrombosis, and Vascular Biology
|July 28, 2007
PubMed
Abstract

Insights

Chronic immune responses to persistent viral antigens in blood vessels significantly worsen atherosclerosis. This study in mice shows that specific T cell reactivity against pathogen-derived antigens accelerates plaque formation.

Area of Science:

  • Immunology
  • Cardiovascular Science
  • Virology

Background:

  • Atherosclerosis is a chronic inflammatory disease.
  • Murine cytomegalovirus (MCMV) infection can accelerate atherosclerosis.
  • The role of specific immune responses against viral antigens in this process is not fully understood.

Purpose of the Study:

  • To investigate the contribution of immunopathological mechanisms in MCMV-accelerated atherogenesis.
  • To differentiate between systemic immune activation and specific immune reactivity against vascular-persisting antigens.

Main Methods:

  • Used apolipoprotein E-deficient (apoE-/-) mice and transgenic mice (apoE-/- x SM-LacZ) expressing beta-galactosidase (beta-gal) in the cardiovascular system.
  • Infected mice with a beta-gal-recombinant MCMV (MCMV-LacZ).
  • Assessed cellular immune responses, T cell expansion, and atherosclerosis development.

Main Results:

  • Both mouse strains showed comparable cellular immune responses to MCMV-LacZ infection.
  • Beta-gal-specific CD4+ T cells expanded and persisted in both groups.
  • Mice with vascular beta-gal expression (apoE-/- x SM-LacZ) exhibited dramatically accelerated atherosclerosis compared to apoE-/- mice.
  • Inflammatory infiltrates were prominent in atherosclerotic lesions of infected apoE-/- x SM-LacZ mice but not in apoE-/- mice.

Conclusions:

  • Chronic immune reactivity against pathogen-derived antigens persisting in the vasculature significantly exacerbates atherogenesis.
  • Specific immune responses targeting vascular-associated antigens play a critical role in accelerating atherosclerosis during viral infection.

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