Vascular lesions in mice with a deficit in Fas-mediated apoptosis and their transfer

Masato Nose, Mitsuko R. Ito, Masao Ono, Shizuko Terasaki, Masaaki Miyazawa, Shiro Mori

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

The lpr and gld genes are thought to result in an incapacity for Fas-mediated apoptosis of T and B cells and the development of subsequent autoimmune disease. A newly established gld-congenic strain of mice, MRL/MpTn-gld/gld (MRL/gld), was found to develop vascular lesions involving arteritis and glomerulonephritis (GN), which were similar to those observed in the MRL/Mp-lpr/lpr (MRL/lpr) strain. However, comparative studies with a C3H/HeJ strain bearing lpr or gld revealed that these lesions developed only in mice with an MRL background. We were successful in transferring GN to normal MHC-compatible gld/gld and irradiated +/+ mice by bone marrow cells of MRL/gld mice, but were unsuccessful using those of C3H/gld mice. Transfer of arteritis, however, was only successful in mice with an MRL background. Nephritogenic monoclonal antibodies obtained from an MRL/lpr and an MRL/gld mouse were shown to be bone marrow-derived and rich in clonal diversity, and at least two of these were capable of causing glomerular injury by different mechanisms. Development of GN and systemic arteritis in MRL/lpr and MRL/gld mice will be dependent not only on their incapacity for Fas-mediated apoptosis but also on bone marrow cells and peripheral cells with intrinsic defects.

Original languageEnglish
Pages (from-to)S35-S44
JournalInternational Journal of Cardiology
Volume54
Issue numberSUPPL.
DOIs
Publication statusPublished - 1996 Aug

Keywords

  • Arteritis
  • Autoimmune disease
  • Fas ligand mutant
  • Fas mutant
  • Glomerulonephritis
  • Nephritogenic antibodies

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

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