IFN-gamma transgenic mice: clues to the pathogenesis of systemic lupus erythematosus?

Description

Transgenic mice overexpressing IFN-γ in the epidermis develop an inflammatory skin disease resembling cutaneous lupus erythematosus shortly after birth. By 3 months of age, most female transgenics develop a lupus-like syndrome characterised by production of IgG anti-dsDNA, antihistone and antinucleosome autoantibodies. The autoantibodies are nephritogenic, with one-third of females developing a severe immune complex mediated glomerulonephritis. Analysis of these transgenics suggests that pathogenic autoantibodies arise via an antigen-driven T-cell-dependent mechanism with apoptotic keratinocytes acting as a potential source of autoantigen. The mechanism of autoantibody production in IFN-γ transgenics may be relevant to human lupus and is consistent with a central role for cutaneous T cells in the pathogenesis of systemic lupus erythematosus in man.

Resources

Name Format Description Link
21 Visit the original government dataset for complete information, documentation, and data access. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC128871/

Tags

  • systemic-lupus-erythematosus
  • ifn-gamma
  • nih
  • autoantibodies
  • transgenic-mice

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