Original Data
| Rev Diabet Stud,
2009,
6(2):104-116 |
DOI 10.1900/RDS.2009.6.104 |
Allelic Variation of Ets1 Does Not Contribute to NK and NKT Cell Deficiencies in Type 1 Diabetes Susceptible NOD Mice
Margaret A. Jordan1, Lynn D. Poulton2, Julie M. Fletcher1, Alan G. Baxter1
1Comparative Genomics Centre, Molecular Sciences Bldg 21, James Cook University, Townsville, QLD 4811, Australia
2Sir William Dunn School of Pathology, University of Oxford, South Parks Road, Oxford, OX1 3RE, United Kingdom
Address correspondence to: Alan G. Baxter, e-mail: alan.baxter@jcu.edu.au
Manuscript submitted July 24, 2009; resubmitted August 4, 2009; accepted August 8, 2009.
Keywords: type 1 diabetes, NK cell, natural killer cell, NKT cell, NOD mouse , Ets1, natural immunity, v-ets, erythroblastosis virus E26 oncogene
Abstract
The NOD mouse is a well characterized model of type 1 diabetes that shares several of the characteristics of Ets1-deficient targeted mutant mice, viz: defects in TCR allelic exclusion, susceptibility to a lupus like disease characterized by IgM and IgG autoantibodies and immune complex-mediated glomerulonephritis, and deficiencies of NK and NKT cells. Here, we sought evidence for allelic variation of Ets1 in mice contributing to the NK and NKT cell phenotypes of the NOD strain. ETS1 expression in NK and NKT cells was reduced in NOD mice, compared to C57BL/6 mice. Although NKT cells numbers were significantly correlated with ETS1 expression in both strains, NKT cell numbers were not linked to the Ets1 gene in a first backcross from NOD to C57BL/6 mice. These results indicate that allelic variation of Ets1 did not contribute to variation in NKT cell numbers in these mice. It remains possible that a third factor not linked to the Ets1 locus controls both ETS1 expression and subsequently NK and NKT cell phenotypes.
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