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The Journal of Immunology, 2005, 174: 6764-6771.
Copyright © 2005 by The American Association of Immunologists

A Defect in Lineage Fate Decision during Fetal Thymic Invariant NKT Cell Development May Regulate Susceptibility to Type 1 Diabetes1

Melany J. D. Wagner*, Shabbir Hussain*, Mala Mehan{ddagger}, Joseph M. Verdi{ddagger} and Terry L. Delovitch2,*,{dagger}

* Autoimmunity/Diabetes, Robarts Research Institute and {dagger} Department of Microbiology and Immunology, University of Western Ontario, London, Ontario Canada; and {ddagger} Center for Regenerative and Molecular Medicine, Maine Medical Center Research Institute, Scarborough, ME 04074

A numerical and functional deficiency in invariant NKT (iNKT) cells detectable by 3 wk of age in the thymus and spleen mediates the pathogenesis of type 1 diabetes in NOD mice, but the stage of T cell development at which this deficiency first occurs is unknown. We report in this study that this deficiency develops after the CD4+CD8+ double-positive stage of thymic T cell development and is due to a lineage-specific depletion of CD4–CD8– double-negative {alpha}{beta} T cells and iNKT cells from the thymus between embryonic day 18 and day 1 after birth. Thus, an inheritable defect in a lineage fate decision that elicits a deficiency in fetal thymic iNKT cell development may predispose to susceptibility to type 1 diabetes.




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