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Mouse Model of Alloimmune-induced Vascular Rejection and Transplant Arteriosclerosis
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Genomics of vasculitis: lessons from mouse models.

Masato Nose1, Hiroaki Komori, Tatsuhiko Miyazaki

  • 1Department of Pathogenomics, Ehime University Graduate School of Medicine, Ehime, Japan ; Department of Immunopathology, Ehime Proteo-Medicine Research Center, Ehime, Japan.

Annals of Vascular Diseases
|May 4, 2013
PubMed
Summary

Systemic vasculitis develops from multiple gene interactions, not single genes, in a polygenic network. This additive genetic effect influences disease development and variation in mouse models.

Keywords:
Cd72MRL micecollagen diseasegenetic polymorphismrecombinant inbred strains

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Area of Science:

  • Genetics
  • Immunology
  • Rheumatology

Background:

  • Systemic vasculitis presents complex clinicopathological features.
  • Understanding the genetic basis of systemic vasculitis is crucial.

Purpose of the Study:

  • To investigate the genetic architecture of systemic vasculitis using mouse models.
  • To identify susceptibility loci and understand their contribution to disease development.

Main Methods:

  • Genome analysis in MRL mouse models.
  • Study of susceptibility loci for vasculitis.
  • Identification of positional candidate genes.

Main Results:

  • Systemic vasculitis arose from the cumulative effect of multiple gene loci (polygenic system).
  • Susceptibility loci acted in an additive manner with hierarchical effects.
  • Some loci were common to other collagen diseases, and tissue-specific loci were identified.
  • A positional candidate gene exhibited allelic polymorphism, suggesting functional differences.

Conclusions:

  • A polygene network, involving combinations of genes with allelic variations, likely drives vasculitis development and variation.
  • This polygenic network model provides insight into the pathogenesis of systemic vasculitis.