Treatment of (NZB x NZW)F1 disease with anti-I-A monoclonal antibodies.
(NZB x NZW)F1 mice spontaneously develop an autoimmune syndrome characterized by a fatal immune complex glomerulonephritis. Administration of monoclonal antibodies specific for an I region gene product (I-Az) of the H-2 haplotype associated with susceptibility to glomerulonephritis in these animals produced a remission in female mice with established renal disease. The results demonstrated that anti-I-A therapy stabilized the level of proteinuria and increased the 1-yr survival rate from 10% to greater than 90% in treated animals relative to control mice. These findings may ultimately have therapeutic potential for the treatment of systemic lupus erythematosus.
D000818:Animals; D000911:Antibodies, Monoclonal / Q000008:administration & dosage*; D001835:Body Weight; D004195:Disease Models, Animal; D005260:Female; D000949:Histocompatibility Antigens Class II / Q000276:immunology*; D008180:Lupus Erythematosus, Systemic / Q000150:complications / Q000276:immunology / Q000628:therapy*; D051379:Mice; D008814:Mice, Inbred NZB; D011507:Proteinuria / Q000209:etiology
D000911:Antibodies, Monoclonal; D000949:Histocompatibility Antigens Class II