Vasculitis-susceptible genes in mice with a deficit in Fas-mediated apoptosis

Masato Nose, Miho Terada, Miyuki Nishihara, Junji Kamogawa, Tatsuhiko Miyazaki, Shiro Mori, Masahiko Nishimura, Yun Wang, Toshiyuki Kamoto, Hiroshi Hiai

Research output: Contribution to journalArticlepeer-review

5 Citations (Scopus)

Abstract

Autoimmune diseases show complex pathological manifestations, which frequently involve systemic vasculitis. This complication is understood to be a manifestation of advanced disease, or to represent distinct entities, restricted by genetic and/or environmental factors. An MRL/Mp strain of mice beating the Fas deletion mutant gene, lpr (MRL/lpr), spontaneously develop systemic vasculitis coincidentally with glomerulonephritis, arthritis and sialoadenitis, but a C3H/HeJ-lpr/lpr (C3H/lpr) strain does not. Thus, this is a suitable model for analyzing the genetic basis of vasculitis in autoimmune diseases. To genetically dissect these complex pathological manifestations, a linkage analysis of each lesion with polymorphic microsatellite markers was performed by using MRL/lprX(MRL/lprX C3H/lpr)F1 backcross mice. Vasculitis- susceptible gene loci were mapped on chromosomes 3 and 4, which were not associated with glomerulonephritis, arthritis and sialoadenitis. These results indicate that systemic vasculitis in MRL/lpr mice may be under the control of host genes which are different from those for other autoimmune diseases.

Original languageEnglish
Pages (from-to)S37-S41+S43
JournalInternational Journal of Cardiology
Volume66
Issue numberSUPPL. 1
DOIs
Publication statusPublished - 1998 Oct 1

Keywords

  • Apoptosis
  • Arteritis
  • Arthritis
  • Disease-susceptible gene
  • Fas
  • Fas ligand
  • Glomerulonephritis
  • MRL mice
  • Sialoadenitis

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

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