作者: Shozo Izui
DOI: 10.14842/JPNJNEPHROL1959.37.610
关键词:
摘要: Genetic analysis of systemic lupus erythematosus (SLE) in several lupus-prone mice has revealed that multiple, unlinked genes are required for the expression various autoimmune manifestations, and several, quite distinct genetic backgrounds compatible with this disease. Although nature these components not been fully defined, it is becoming clear certain such as major histocompatibility complex class II regulating apoptosis apparently play a role development responses characteristic SLE. Analysis nephritogenic potential monoclonal autoantibodies underlines importance qualitative features pathogenesis nephritis. Strikingly, "wire-loop" glomerular lesions human nephritis can be induced by direct localization murine IgG3 antibodies cryoglobulin activity without involvement immune formation. The remarkable correlation production acceleration nephritis, association enhanced activation TH1 subset which lead to an increase production, highly significant. process more pathogenic appears genetically regulated. Further identification defects present mice, but lacking non-autoimmune backgrounds, paramount understanding immunopathogenetic mechanism new therapeutic approaches