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

Authors
Journal
International Journal of Cardiology
0167-5273
Publisher
Elsevier
Publication Date
Volume
54
Identifiers
DOI: 10.1016/0167-5273(96)02636-8
Keywords
  • Fas Mutant
  • Fas Ligand Mutant
  • Autoimmune Disease
  • Arteritis
  • Glomerulonephritis
  • Nephritogenic Antibodies
Disciplines
  • Medicine

Abstract

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 (MRU/ lpr) strain. However, comparative studies with a C3H/HeJ strain bearing Ipr 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 MRU 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.

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