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  • 1
    Electronic Resource
    Electronic Resource
    RFLP analysis of the MHC class III region defines unique haplotypes for the non-obese diabetic, cataract Shionogi and the non-obese non-diabetic mouse strains (1993)
    Springer
    Diabetologia 36 (1993), S. 727-733 
    Details
    ISSN: 1432-0428
    Keywords: MHC class III region ; non-obese diabetic mouse ; non-obese non-diabetic mouse ; cataract Shionogi mouse ; Type 1 (insulin-dependent) diabetes mellitus ; restriction fragment length polymorphisms
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The non-obese diabetic (NOD) mouse strain which spontaneously develops diabetes is a model for human Type 1 (insulin-dependent) diabetes mellitus. At least one of several genes controlling diabetes in the NOD mouse has been mapped to the MHC. Although previous experiments have implicated the MHC class II genes in the development of the disease, the existence of other MHC linked susceptibility genes has not been ruled out. In order to identify these susceptibility genes we have further characterized the MHC haplotype of the NOD mouse and two non-diabetic sister strains, the non-obese non-diabetic (NON) and cataract Shionogi (CTS). We have examined the mouse MHC class III region for the presence of homologous genes to 17 newly isolated human MHC class III region genes (G1, G2, G4, G6, G7a/valyl-tRNA synthetase, HSP70, G8, G9, G10, G12, G13, G14, G15, G16, G17 and G18). We detect unique hybridizing DNA fragments for 16 of the 17 genes in six inbred mouse strains (NOD, NON, CTS, B10, BALB/c and CBA/J) indicating that this part of the H-2 region is similar to the human MHC class III region. Using a panel of restriction enzymes we have defined RFLPs for 6 (G2, G6, HSP70, G12, G16, G18) of the 16 cross-hybridizing probes. The RFLPs demonstrate that NOD, NON and CTS mouse strains each have a distinct MHC haplotype in the MHC class III region.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00401143
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    The cataract Shionogi mouse, a sister strain of the non-obese diabetic mouse: similar class II but different class I gene products (1988)
    Springer
    Diabetologia 31 (1988), S. 254-258 
    Details
    ISSN: 1432-0428
    Keywords: Major histocompatibility complex ; non-obese diabetic mouse ; non-obese non-diabetic mouse ; cataract Shionogi mouse ; insulin-dependent diabetes ; restriction fragment length polymorphisms
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We have studied with a series of monoclonal antibodies and restriction fragment analysis the K, D, and class II region of the major histocompatibility complex of the non-obese diabetic mouse in comparison with its sister strains, the non-obese non-diabetic and cataract Shionogi mouse. (1) K region: Monoclonal antibody 31-3-4S (anti-Kd) reacted with splenocytes from non-obese diabetic mice while other anti-K (Kb, Kk, Kq) monoclonals did not react. Splenocytes from non-obese non-diabetic mice reacted with both anti-Kb and Kk monoclonals while splenocytes from cataract Shionogi mice reacted with anti-Kd and Kk monoclonals. Both sister strains, therefore, differ from the non-obese diabetic and other known mice strains by monoclonal analysis of H-2K. (2) D region: Splenocytes from both non-obese diabetic and non-obese non-diabetic mice reacted with monoclonal antibody 28-14-8S (anti-Db) while splenocytes from cataract Shionogi mice did not react with any anti-D monoclonal antibody tested. (3a) Class II region (non-obese diabetic and non-obese non-diabetic mice): Three of 11 monoclonal antibodies to class II molecules reacted with splenocytes of the non-obese diabetic mouse. The 3 reacting monoclonals have I-Ak primary specificities though additional anti-I-Ak monoclonal antibodies were negative. Among these monoclonals, 39B and 40A reacted with the non-obese diabetic mouse but not with the non-obese non-diabetic mouse, while 10-2-16 reacted with non-obese diabetic, non-obese non-diabetic and cataract Shionogi mice. Monoclonal MKD6 (anti-I-Ad) reacted with non-obese non-diabetic but not non-obese diabetic mice. In crosses of non-obese diabetic with non-obese non-diabetic mice, splenocytes from all diabetic backcrosses studied (6/6) were positive with monoclonal 40A but negative with MKD6 indicating that the major histocompatibility complex of non-obese non-diabetic mice is not diabetogenic and confirming major histocompatibility complex-linkage of the diabetogenic gene in this additional cross. (3b) Class II region (cataract Shionogi mice): Utilising 11 anti-class II monoclonal antibodies the pattern of reactivity of the cataract Shionogi mouse was identical to the non-obese diabetic mouse. Splenocytes from both non-obese diabetic and cataract Shionogi mice fail to express I-E (no reaction with monoclonal 14-4-4). In addition, using an I-A alpha probe with restriction endonuclease HindIII or I-A beta probe with BamHI, the restriction fragment length polymorphism pattern of the cataract Shionogi mouse was identical to the non-obese diabetic mouse. In summary, the cataract Shionogi mouse appears to have a similar I-A region to the non-obese diabetic mouse but differs at both the K and D region. With the hypothesis that the unique I-A beta of the non-obese diabetic mouse is diabetogenic, the cataract Shionogi mouse should provide a new strain for further characterisation of diabetogenic genes of the non-obese diabetic mouse since it is similar at I-A, fails to express I-E, but differs at both class I loci.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00290594
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    Paper (German National Licenses)
    Fulltext
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