First Author | Tsaih SW | Year | 2013 |
Journal | Genes Immun | Volume | 14 |
Issue | 6 | Pages | 380-6 |
PubMed ID | 23719031 | Mgi Jnum | J:308404 |
Mgi Id | MGI:6726693 | Doi | 10.1038/gene.2013.32 |
Citation | Tsaih SW, et al. (2013) Genetic control of murine invariant natural killer T cells maps to multiple type 1 diabetes regions. Genes Immun 14(6):380-6 |
abstractText | Reduced frequency of invariant natural killer T (iNKT) cells has been indicated as a contributing factor to type 1 diabetes (T1D) development in NOD mice. To further understand the genetic basis of the defect, we generated (NOD x ICR)F2 mice to map genes that control iNKT-cell development. We determined frequencies of thymic and splenic iNKT cells, as well as the ratio of CD4-positive and -negative subsets in the spleens of 209 F2 males. Quantitative trait loci (QTL) analysis revealed five loci that exceed the significant threshold for the frequency of thymic and/or splenic iNKT cells on Chromosomes (Chr) 1, 5, 6, 12 and 17. Three significant loci on Chr 1, 4 and 5 were found for the ratio of CD4-positive and -negative splenic iNKT cells. Comparisons with previously known mouse T1D susceptibility (Idd) loci revealed two significant QTL peak locations, respectively, mapped to Idd regions on Chr 4 and 6. The peak marker location of the significant Chr 12 iNKT QTL maps to within 0.5 Mb of a syntenic human T1D locus. Collectively, our results reveal several novel loci controlling iNKT-cell development and provide additional information for future T1D genetic studies. |