Abstract
Predisposition to Type I insulin-dependent diabetes (IDD) has a strong underlying genetic basis involving class II major histocompatibility complex (MHC) genes as well as several non-MHC genetic systems. In the non-obese diabetic (NOD) mouse, a model for human IDD, genes associated with the appearance of immune cell infiltrates in the pancreatic islets (insulitis) and/or overt IDD have been mapped to chromosomes 1, 3, 6, 11, and 17. A recent report has suggested that CD8+ lymphocytes of the NOD mouse might be deficient in the expression of the CD8ß molecule, a protein encoded by a gene on chromosome 6. The CD8ß molecule is a T-cell surface marker, the lack of which could affect selection in the thymus, possibly permitting auto-reactive T-cell clones to populate the peripheral lymphoid tissues. For this reason, we examined the expression of the CD8 molecule by lymphocytes in the NOD mouse. Results indicate that the NOD mouse is not deficient in its transcription of detectable mRNA encoding either the CD8α or ß subunits. However, the NOD mouse expresses the Lyt2 a and Lyt3 a alleles, suggesting that a portion of chromosome 6 centromeric to the diabetes-susceptibility genetic region is derived from an ancestry common to AKR and, like AKR, the CD8α and CD8ß3.1 (but not CD8ß3.2) subunits are detected on the cell surface of T lymphocytes of the NOD mouse. Interestingly, though, the CD8ß3.1 molecule may not be expressed in the NOD mouse to the same extent as it is expressed in the AKR/J mouse, suggesting the possibility that the NOD mouse possesses a defect somewhere between transcription and cell surface expression of the CD8ß molecule
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The nucleotide sequence data reported in this paper have been submitted to the EMBL/GenBank nucleotide sequence databases and have been assigned the accession numbers U34881 and U34882
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Johnson-Tardieu, J.M., Walworth, E.W., Cornelius, J.G. et al. Autoimmune diabetes-prone NOD mice express the Lyt2 a (Lyt2.1) and Lyt3 a (Lyt3.1) alleles of CD8. Immunogenetics 43, 6–12 (1995). https://doi.org/10.1007/BF00186598
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DOI: https://doi.org/10.1007/BF00186598