| First Author | Kawano H | Year | 1992 |
| Journal | Clin Immunol Immunopathol | Volume | 65 |
| Issue | 3 | Pages | 308-14 |
| PubMed ID | 1451334 | Mgi Jnum | J:3381 |
| Mgi Id | MGI:51894 | Doi | 10.1016/0090-1229(92)90162-h |
| Citation | Kawano H, et al. (1992) Heterozygosity of the major histocompatibility complex controls the autoimmune disease in (NZW x BXSB) F1 mice. Clin Immunol Immunopathol 65(3):308-14 |
| abstractText | In the F1 hybrid of phenotypically normal NZW (H-2z) and systemic lupus erythematosus (SLE)-prone BXSB mice (H-2b), features of the disease became more severe than those seen in the BXSB mice, regardless of the presence or absence of the Yaa (Y-chromosome-linked autoimmune acceleration) mutant gene. To determine whether the gene(s) linked to the major histocompatibility complex (MHC) of NZW mice is involved in this event, we developed the H-2-congenic NZW.H-2d strain and compared the severity of autoimmune disease between (NZW x BXSB) F1 (H-2z/b) and (NZW.H-2d x BXSB) F1 mice (H-2d/b). The H-2z/b, but not H-2d/b, heterozygous F1 mice of both sexes showed an accelerated, higher incidence of proteinuria and a more severe thrombocytopenia than did the BXSB mice. In NZW x (NZW x BXSB) F1 backcross mice, the H-2z/b heterozygous progeny showed more severe disease than did the H-2z/z homozygotes. Thus, disease-accelerating events in (NZW x BXSB) F1 mice are linked to the H-2z/b heterozygosity. Because H-2d/z heterozygosity plays a crucial role for SLE in (NZB x NZW) F1 mice, in which SLE features differ from those in (NZW x BXSB) F1 mice, the present observations may imply that the different but related MHC heterozygosity acts as a predisposing genetic element in these different SLE syndromes. |
