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Scientific article
English

Anti-IgM treatment of C57BL/6-1pr/1pr mice: depletion of B cells reduces 1pr gene-induced lymphoproliferation and mononuclear cell vasculitis

Published inClinical and experimental immunology, vol. 77, no. 1, p. 124-129
Publication date1989
Abstract

In order to study the role of B cells in autoimmune abnormalities observed in C57BL/6 mice bearing the autosomal mutant gene 1pr (lymphoproliferation), we treated mice from birth continuously with rabbit anti-IgM antiserum. Anti-IgM treatment resulted in the complete suppression of B cell development, documented by the absence of surface Ig-positive cells, the lack of lipopolysacchride-induced mitogenic responses, and the lack of autoantibody production. Although, anti-IgM-treated C57BL/6-1pr/1pr mice developed 1pr gene-associated lymphoproliferation due to the accumulation of Thy-1+, CD4-, CD8-, B220+ T lymphocytes in spleen and lymph nodes, the size of their spleen and lymph nodes was considerably smaller than that of normal rabbit serum-treated C57BL/6-1pr/1pr mice. Systemic vascular lesions associated with mononuclear cell infiltration were a little affected by anti-IgM treatment. This indicates that the development of mononuclear cell vasculitis in mice bearing the 1pr gene may be associated with the 1pr gene-induced lymphoproliferation and is independent of B cells and autoantibody production.

Keywords
  • Animals
  • Antibodies, Anti-Idiotypic/immunology
  • Autoantibodies/biosynthesis
  • Autoimmune Diseases/immunology
  • B-Lymphocytes/ immunology
  • Immunoglobulin M/immunology
  • Lymphocyte Activation
  • Lymphocyte Depletion
  • Mice
  • Mice, Inbred C57BL
  • Mice, Mutant Strains
  • Mutation
  • Vasculitis/ immunology
Affiliation Not a UNIGE publication
Citation (ISO format)
CERNY, A. et al. Anti-IgM treatment of C57BL/6-1pr/1pr mice: depletion of B cells reduces 1pr gene-induced lymphoproliferation and mononuclear cell vasculitis. In: Clinical and experimental immunology, 1989, vol. 77, n° 1, p. 124–129.
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ISSN of the journal0009-9104
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