International Mammalian Genome Society

The 15th International Mouse Genome Conference (2001)


Dr Tom Brodnicki
The Walter & Eliza Hall Institute
Post Office Royal Melbourne Hospital
Melbourne 3050 Australia

Co-Authors:  McClive P, Couper S, and Morahan G
Institution:   The Walter & Eliza Hall Institute

Type 1 diabetes is a multigenic autoimmune disease.  The reason(s) autoreactive T cells become activated and mediate destruction of insulin-producing beta cells are not fully understood, but insights may be gained from the nonobese diabetic (NOD) mouse.  We previously located a NOD diabetes susceptibility locus, designated Idd11, on mouse chromosome 4 by analyzing diabetic backcross mice produced after crossing NOD/Lt with the nondiabetic resistant C57BL/6 (B6) strain.  In order to confirm Idd11 and further refine its location, three NOD congenic mouse strains with different B6-derived intervals within chromosome 4 were generated.  Two of the congenic strains had a significant decrease in the cumulative incidence of diabetes compared to NOD/Lt control mice.  The third NOD congenic strain, containing a B6 interval surrounding the Slc9a1 locus, was not protected against diabetes.  Mouse chromosome 4 has also been linked to another autoimmune disease, systemic lupus erythematosus (SLE), in the New Zealand Black (NZB) mouse strain.  Another mouse strain was generated which contained one copy of the NZB interval for Idd11 on the NOD background.  Analysis of this mouse strain demostrated that the NZB interval for Idd11, compared to the B6 interval, is unable to protect NOD mice from diabetes.  These combined results define a new distal boundary for Idd11 and suggest that the Idd11 locus may play a role in SLE development.

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