Insulin-dependent diabetes loci Idd5 and Idd9 increase sensitivity to experimental autoimmune encephalomyelitis
Copyright policy )Insulin-dependent diabetes loci Idd5 and Idd9 increase sensitivity to experimental autoimmune encephalomyelitis
The spontaneous development of autoimmune diabetes in NOD mice suggests that they are unable to establish and maintain immunologic self-tolerance. Congenic NOD mice expressing B10-derived alleles are protected from pancreatic beta cell destruction and autoimmune diabetes. To determine if the B10 alleles in loci Idd5 and Idd9 could influence susceptibility to autoimmunity in other organs, we compared MOG35-55-induced EAE in NOD mice to that of diabetes-resistant NOD.B10.Idd5 and NOD.B10.Idd9 mice. Surprisingly, the severity and chronicity of EAE were enhanced in the diabetes-resistant congenic mice. Our findings indicate that some alleles may influence susceptibility to immune-mediated damage in an organ or tissue-specific fashion, and highlight the necessity of disease-specific investigations.
- University System of Ohio United States
- Torrey Pines Institute For Molecular Studies United States
- University of Toledo United States
Encephalomyelitis, Autoimmune, Experimental, Incidence, T-Lymphocytes, Receptors, Antigen, T-Cell, Severity of Illness Index, Peptide Fragments, Mice, Diabetes Mellitus, Type 1, Animals, Congenic, Mice, Inbred NOD, Animals, Cytokines, Genetic Predisposition to Disease, Myelin-Oligodendrocyte Glycoprotein, Cells, Cultured, Glycoproteins
Encephalomyelitis, Autoimmune, Experimental, Incidence, T-Lymphocytes, Receptors, Antigen, T-Cell, Severity of Illness Index, Peptide Fragments, Mice, Diabetes Mellitus, Type 1, Animals, Congenic, Mice, Inbred NOD, Animals, Cytokines, Genetic Predisposition to Disease, Myelin-Oligodendrocyte Glycoprotein, Cells, Cultured, Glycoproteins
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