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Major Histocompatibility Complex–Linked Diabetes Susceptibility in NOD/Lt Mice

Subcongenic Analysis Localizes a Component of Idd16 at the H2-D End of the Diabetogenic H2^g7 Complex

¹ The Jackson Laboratory, Bar Harbor, Maine
² University of Pittsburgh, Department of Pediatrics, Pittsburgh, Pennsylvania

The diabetogenic major histocompatibility complex (MHC) (H2^g7) of NOD mice comprises contributions from several class II loci collectively designated as Idd1. Introduction of the H2^gx haplotype from the related but diabetes-resistant cataract Shionogi (CTS) strain demonstrated an additional MHC-linked locus designated Idd16. The NOD-related alloxan resistant (ALR)/Lt strain is also characterized by the H2^gx haplotype, which does not differ from H2^g7 from the class I H2-K^d gene distally through the class II and into the class III region. Polymorphisms distal to the heat shock protein 70 locus (Hspa1b) include a rare H2-D^dx rather than the H2^g7 encoded D^b allele. Two differential-length NOD.ALR-H2^gx congenic stocks (D.R1 and D.R2), both containing H2-D^dx, significantly suppressed diabetogenesis. This protection was lost when ALR alleles between the class III region and H2-D were removed in a shorter interval congenic (D.R3). Because no differences were observed in the ALR-derived interval extending 0.41 mB proximal to H2-K in any of these congenic stocks, a component of what was originally designated "Idd16" was sited to an interval shorter than 7.33 mB, distinguishing D.R2 from D.R3. Evidence supporting the candidacy of the ALR/CTS-shared H2-D^dx MHC class I variant present in both diabetes-resistant stocks, but not the susceptible stock, is discussed.

Abbreviations: ALR, alloxan resistant; CTS, cataract Shionogi; MHC, major histocompatibility complex

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