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Subcongenic analysis of genetic basis for impaired development of invariant NKT cells in NOD mice. Immunogenetics 2007 Sep;59(9):705-12



Pubmed ID




Scopus ID

2-s2.0-34548661992   23 Citations


Reduced numbers and function of invariant NKT (iNKT) cells partially contribute to type 1 diabetes (T1D) development in NOD mice. Previous linkage analysis identified a genetic locus on chromosome 2 controlling numbers of thymic iNKT cells. Interestingly, this locus resides within the Idd13 region that distinguishes NOD mice from the closely genetically related, but strongly T1D-resistant NOR strain. Thus, we tested if a genetic variant that confers T1D resistance in NOR mice may do so by enhancing iNKT cell numbers. iNKT cells were enumerated by an alpha-GalCer analog loaded CD1d tetramer in NOD and NOR mice as well as in NOD stocks carrying NOR-derived congenic regions on chromosome 1, 2, or 4. Significantly, more thymic and splenic iNKT cells were present in NOR than NOD mice. The NOR-derived Idd13 region on chromosome 2 contributed the most significant effect on increasing iNKT cell numbers. Subcongenic analyses indicated that at least two genes within the Idd13 region regulate iNKT cell numbers. These results further define the genetic basis for numerical iNKT cell defects contributing to T1D development in NOD mice.

Author List

Chen YG, Driver JP, Silveira PA, Serreze DV


Yi-Guang Chen PhD Professor in the Pediatrics department at Medical College of Wisconsin

MESH terms used to index this publication - Major topics in bold

Antigens, CD1
Diabetes Mellitus, Type 1
Genetic Predisposition to Disease
Killer Cells, Natural
Lymphocyte Activation
Lymphocyte Count
Mice, Congenic
Mice, Inbred NOD
Species Specificity