作者: Chaim O. Jacob , Hugh O. McDevitt
DOI: 10.1038/331356A0
关键词: Tumor necrosis factor alpha 、 Lupus nephritis 、 Biology 、 Major histocompatibility complex 、 Immunology 、 Allele 、 Pathogenesis 、 Nephritis 、 Autoimmune disease 、 Necrosis
摘要: The (NZB x NZW)F1 hybrid mouse develops a severe autoimmune disease similar to systemic lupus erythematosus in humans. Both the human and murine form of show strong associations with alleles major histocompatibility complex (MHC) gene products. found F1 mice is due, part, dominant NZW gene(s) mapping H-2 (the MHC). Here we present evidence that tumour necrosis factor (TNF-alpha) gene, which located within complex), could be involved pathogenesis nephritis mice. Thus, restriction fragment length polymorphism TNF-alpha correlates reduced levels produced by Furthermore, replacement therapy recombinant induces significant delay development nephritis.