title: Requirement of H-2 heterozygosity for autoimmunity in (NZB X NZW)F1 hybrid mice.
abstract: In the F1 hybrid of autoimmune New Zealand Black (NZB) and phenotypically normal New Zealand White (NZW) mice, there occurs a severe systemic lupus erythematosus (SLE)-like autoimmune disease more fulminant than that found in the parental NZB mice. To determine the role of the H-2 complex in the pathogenesis of autoimmune disease of the (NZB X NZW)F1 hybrid, we developed H-2-congenic NZB (NZB.H-2z) and NZW (NZW.H-2d) strains, and compared the degree of autoimmune features between congenic H-2d/H-2d and H-2z/H-2z homozygous F1 hybrids and the original H-2d/H-2z heterozygous (NZB X NZW)F1 hybrid. We found that autoimmune features such as productions of IgG class anti-DNA antibodies and retroviral gp70 immune complexes and the development of renal disease were to a great extent reduced in both H-2 homozygous F1 hybrids, as compared with the H-2 heterozygous (NZB X NZW)F1 hybrid. It would thus appear that the heterozygosity of H-2d haplotype derived from NZB and H-2z from NZW is essential for the autoimmune disease characteristic of the (NZB X NZW)F1 hybrid.
mesh_terms: D000818:Animals; D001327:Autoimmune Diseases / Q000235:genetics*; D004247:DNA / Q000276:immunology; D006183:H-2 Antigens / Q000235:genetics*; D006579:Heterozygote; D006824:Hybridization, Genetic; D007074:Immunoglobulin G / Q000032:analysis; D051379:Mice; D008814:Mice, Inbred NZB; D010446:Peptide Fragments / Q000235:genetics; D011948:Receptors, Antigen, T-Cell / Q000235:genetics; D016693:Receptors, Antigen, T-Cell, alpha-beta
chemical_list: D006183:H-2 Antigens; D007074:Immunoglobulin G; D010446:Peptide Fragments; D011948:Receptors, Antigen, T-Cell; D016693:Receptors, Antigen, T-Cell, alpha-beta; D004247:DNA