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Gene Review

Idd5  -  insulin dependent diabetes susceptibility 5

Mus musculus

Synonyms: Idd-5
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Disease relevance of Idd5

  • Insulin-dependent diabetes loci Idd5 and Idd9 increase sensitivity to experimental autoimmune encephalomyelitis [1].
  • In this study, we determined the efficiency with which macrophages from diabetes-prone NOD and diabetes-resistant NOR, Idd5, Balb/c, and C57BL/6 mice phagocytose apoptotic thymocytes and NIT-1 insulinoma cells [2].
  • In the present study, we bred the Idd3 and Idd5 chromosomal intervals from NOD mice into non-autoimmune C57BL/6 mice to determine if these intervals recreate a Sjögren's syndrome (SS)-like phenotype [3].
  • More than 19 chromosomal intervals (referred to as Idd regions) that contribute to diabetes susceptibility in the NOD mouse model have been identified, but only 2 chromosomal intervals (associated with Idd3 and Idd5) have been shown to control sialadenitis [3].

High impact information on Idd5

  • This places it in a region of chromosome 2q that shows conserved synteny with the region of mouse chromosome 1 containing the murine type 1 diabetes gene, Idd5 [4].
  • We report that NOD-derived alleles at both the Idd5 and Idd13 loci regulate a T lymphocyte-dependent progression from a benign to a destructive stage of insulitis [5].
  • Apoptosis resistance of nonobese diabetic peripheral lymphocytes linked to the Idd5 diabetes susceptibility region [6].
  • Congenic strains on both the NOD and NOR backgrounds confirmed the roles of Idd4 and Idd9 in CY-T1D susceptibility and revealed the contribution of a third locus, Idd5 [7].
  • Additional expression studies in this work support the hypothesis that this SNP in exon 2 is the genetic variation causing the biological effects of Idd5 [8].

Biological context of Idd5

  • On its own, the Idd5 locus provides a significant amount of protection from diabetes (50% reduction from parental frequency) and when combined with another resistance locus (Idd3 on chromosome 3), provides nearly complete protection from diabetes and insulitis [9].
  • 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 [1].
  • For Idd3 and Idd5 we would also not reject a model of additivity on the penetrance scale, which might indicate a disease model mediated by more than one pathway leading to beta-cell destruction and development of diabetes [10].
  • 3. The homologues of these genes may reside on human chromosomes 1 or 4 (Idd-3), 17 (Idd-4) and 2q (Idd-5) [11].

Anatomical context of Idd5


Analytical, diagnostic and therapeutic context of Idd5

  • Islet allograft tolerance could not be induced in diabetes-resistant NOD.B10 Idd5 and NOD.B10 Idd9 mice [14].


  1. Insulin-dependent diabetes loci Idd5 and Idd9 increase sensitivity to experimental autoimmune encephalomyelitis. Mayo, S., Kohler, W., Kumar, V., Quinn, A. Clin. Immunol. (2006) [Pubmed]
  2. Phagocytosis of apoptotic cells by macrophages from NOD mice is reduced. O'Brien, B.A., Huang, Y., Geng, X., Dutz, J.P., Finegood, D.T. Diabetes (2002) [Pubmed]
  3. Two NOD Idd-associated intervals contribute synergistically to the development of autoimmune exocrinopathy (Sjögren's syndrome) on a healthy murine background. Cha, S., Nagashima, H., Brown, V.B., Peck, A.B., Humphreys-Beher, M.G. Arthritis Rheum. (2002) [Pubmed]
  4. Linkage disequilibrium mapping of a type 1 diabetes susceptibility gene (IDDM7) to chromosome 2q31-q33. Copeman, J.B., Cucca, F., Hearne, C.M., Cornall, R.J., Reed, P.W., Rønningen, K.S., Undlien, D.E., Nisticò, L., Buzzetti, R., Tosi, R. Nat. Genet. (1995) [Pubmed]
  5. Two genetic loci regulate T cell-dependent islet inflammation and drive autoimmune diabetes pathogenesis. Fox, C.J., Paterson, A.D., Mortin-Toth, S.M., Danska, J.S. Am. J. Hum. Genet. (2000) [Pubmed]
  6. Apoptosis resistance of nonobese diabetic peripheral lymphocytes linked to the Idd5 diabetes susceptibility region. Colucci, F., Bergman, M.L., Penha-Gonçalves, C., Cilio, C.M., Holmberg, D. Proc. Natl. Acad. Sci. U.S.A. (1997) [Pubmed]
  7. Sex-specific effect of insulin-dependent diabetes 4 on regulation of diabetes pathogenesis in the nonobese diabetic mouse. Ivakine, E.A., Fox, C.J., Paterson, A.D., Mortin-Toth, S.M., Canty, A., Walton, D.S., Aleksa, K., Ito, S., Danska, J.S. J. Immunol. (2005) [Pubmed]
  8. Fine mapping, gene content, comparative sequencing, and expression analyses support Ctla4 and Nramp1 as candidates for Idd5.1 and Idd5.2 in the nonobese diabetic mouse. Wicker, L.S., Chamberlain, G., Hunter, K., Rainbow, D., Howlett, S., Tiffen, P., Clark, J., Gonzalez-Munoz, A., Cumiskey, A.M., Rosa, R.L., Howson, J.M., Smink, L.J., Kingsnorth, A., Lyons, P.A., Gregory, S., Rogers, J., Todd, J.A., Peterson, L.B. J. Immunol. (2004) [Pubmed]
  9. NOD Idd5 locus controls insulitis and diabetes and overlaps the orthologous CTLA4/IDDM12 and NRAMP1 loci in humans. Hill, N.J., Lyons, P.A., Armitage, N., Todd, J.A., Wicker, L.S., Peterson, L.B. Diabetes (2000) [Pubmed]
  10. Statistical modeling of interlocus interactions in a complex disease: rejection of the multiplicative model of epistasis in type 1 diabetes. Cordell, H.J., Todd, J.A., Hill, N.J., Lord, C.J., Lyons, P.A., Peterson, L.B., Wicker, L.S., Clayton, D.G. Genetics (2001) [Pubmed]
  11. Genetics of a multifactorial disease: autoimmune type 1 diabetes mellitus. Cornall, R.J. Clin. Sci. (1993) [Pubmed]
  12. CTLA-4-/- mice display T cell-apoptosis resistance resembling that ascribed to autoimmune-prone non-obese diabetic (NOD) mice. Bergman, M.L., Cilio, C.M., Penha-Gonçalves, C., Lamhamedi-Cherradi, S.E., Löfgren, A., Colucci, F., Lejon, K., Garchon, H.J., Holmberg, D. J. Autoimmun. (2001) [Pubmed]
  13. Bone marrow abnormalities in the non-obese diabetic mouse. Langmuir, P.B., Bridgett, M.M., Bothwell, A.L., Crispe, I.N. Int. Immunol. (1993) [Pubmed]
  14. Islet allograft survival induced by costimulation blockade in NOD mice is controlled by allelic variants of Idd3. Pearson, T., Weiser, P., Markees, T.G., Serreze, D.V., Wicker, L.S., Peterson, L.B., Cumisky, A.M., Shultz, L.D., Mordes, J.P., Rossini, A.A., Greiner, D.L. Diabetes (2004) [Pubmed]
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