Requirement of H‐2 heterozygosity for autoimmunity in (NZB × NZW)F1 hybrid mice
Requirement of H‐2 heterozygosity for autoimmunity in (NZB × NZW)F1 hybrid mice
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(NZB × NZW)F1 杂交小鼠自身免疫的 H−2 杂合性要求
DOI:
10.1002/eji.1830161226
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发表时间:
1986
影响因子:
5.4
通讯作者:
T. Shirai
中科院分区:
文献类型:
--
作者:
Short Paper;S. Hirose;G. Ueda;K. Noguchi;T. Okada;I. Sekigawa;H. Sato;T. Shirai
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 × 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 × 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 × 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 × NZW)F1 hybrid.