An experimental autoimmune diabetes in mice characterized by delayed-onset hyperglycemia with lymphocytic infiltrations of the pancreatic islets can be induced by multiple administrations of low doses of streptozocin (STZ). We report on the influence of the MHC (H-2 complex) on this autoimmune diabetes by comparing the susceptibilities of various congenic and recombinant strains with a B10 background. In congenic strains, C57BL/10 (H-2b) and B10.BR (H-2k) mice showed a high incidence of diabetes, whereas B10.D2 (H-2d) and B10.S (H-2S) mice showed a low incidence. Therefore, we suggest that the H-2 complex influences diabetes susceptibility and that both b and k are high-susceptibility alleles, whereas d and s are low-susceptibility alleles. In recombinant strains, those with the same haplotypes on the K E S, and D subregions of the H-2 complex showed undefined (high and low) susceptibilities, indicating that the diabetes-susceptibility genes are located outside these loci. Strains possessing I-Ab or I-Ak gene products (C57BL/10, B10.BR, B10.TL, B10.A, and B10.A(2R)) showed high incidences, whereas strains possessing I-Ad or I-As (B10.D2, B10.S, B10.S(7R), B10.S(9R), and B10.GD) showed low incidences. In addition, administration of anti-1-M monoclonal antibody prevented the manifestation of diabetes in STZadministered mice. Passive transfer of STZadministered T lymphocytes to mice given minute doses of STZ induced significant hyperglycemia. This successful transfer was only observed in H-2–compatible mice. Thus, we conclude that one gene coding for susceptibility to this experimental diabetes was located in the I-A subregion within the H-2 complex.
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Original Articles|
October 01 1990
Genetic Control by I-A Subregion in H-2 Complex of Incidence of Streptozocin-Induced Autoimmune Diabetes in Mice
Shun-Ichi Tanaka;
Shun-Ichi Tanaka
Third Department of Internal Medicine, the Second Department of Pathology, and the Department of Bacteriology, Yokohama City University School of Medicine
Yokohama
Fujisawa City Hospital
Fujisawa, Japan
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Shigeru Nakajima;
Shigeru Nakajima
Third Department of Internal Medicine, the Second Department of Pathology, and the Department of Bacteriology, Yokohama City University School of Medicine
Yokohama
Fujisawa City Hospital
Fujisawa, Japan
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Shuji Inoue;
Shuji Inoue
Third Department of Internal Medicine, the Second Department of Pathology, and the Department of Bacteriology, Yokohama City University School of Medicine
Yokohama
Fujisawa City Hospital
Fujisawa, Japan
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Yutaro Takamura;
Yutaro Takamura
Third Department of Internal Medicine, the Second Department of Pathology, and the Department of Bacteriology, Yokohama City University School of Medicine
Yokohama
Fujisawa City Hospital
Fujisawa, Japan
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Ichiro Aoki;
Ichiro Aoki
Third Department of Internal Medicine, the Second Department of Pathology, and the Department of Bacteriology, Yokohama City University School of Medicine
Yokohama
Fujisawa City Hospital
Fujisawa, Japan
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Kenji Okuda
Kenji Okuda
Third Department of Internal Medicine, the Second Department of Pathology, and the Department of Bacteriology, Yokohama City University School of Medicine
Yokohama
Fujisawa City Hospital
Fujisawa, Japan
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Address correspondence and reprint requests to Dr. S.-l. Tanaka, the Third Department of Internal Medicine, Yokohama City University School of Medicine, 3-46 Urafune-Cho, Minami-Ku, Yokohama 232, Japan.
Diabetes 1990;39(10):1298–1304
Article history
Received:
June 28 1989
Revision Received:
May 18 1990
Accepted:
May 18 1990
PubMed:
2145188
Citation
Shun-Ichi Tanaka, Shigeru Nakajima, Shuji Inoue, Yutaro Takamura, Ichiro Aoki, Kenji Okuda; Genetic Control by I-A Subregion in H-2 Complex of Incidence of Streptozocin-Induced Autoimmune Diabetes in Mice. Diabetes 1 October 1990; 39 (10): 1298–1304. https://doi.org/10.2337/diab.39.10.1298
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