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The Journal of Immunology, 2003, 170: 5429-5437.
Copyright © 2003 by The American Association of Immunologists

Genetic Dissection of V{alpha}14J{alpha}18 Natural T Cell Number and Function in Autoimmune-Prone Mice1

Naoto Matsuki*, Aleksandar K. Stanic*, Monica E. Embers{dagger}, Luc Van Kaer*, Laurence Morel{ddagger} and Sebastian Joyce2,*

* Department of Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, TN 37232; {dagger} Department of Microbiology and Immunology, Pennsylvania State University College of Medicine, Hershey, PA 17033; and {ddagger} Department of Pathology, University of Florida, Gainesville, FL 32610

Nonobese diabetic (NOD) mice, a model for type I diabetes (TID), have reduced numbers of invariant V{alpha}14J{alpha}18 TCR {alpha}-chain-positive natural T (iNKT) cells that do not release IL-4 in response to in vivo activation through their Ag receptor. The deficit in iNKT cell number and function is implicated in immune dysregulation and the etiology of TID. Therefore, we reasoned that the genetic determinant(s) that controls iNKT cell number and function might lie within Idd (insulin-dependent diabetes susceptibility locus) regions, which are known to contain TID resistance or susceptibility genes. A systematic analysis of iNKT cell number and function in Idd congenic mice revealed that neither iNKT cell number nor their inability to rapidly secrete IL-4 in response to acute in vivo activation by Ag underlies the mechanism of protection from diabetes in Idd congenic mice. Moreover, the regulation of iNKT cell number and function appears to be under the control of several genes. The most notable of these map to the Idd4, Idd5, Idd9.1, and Idd13 regions of the mouse genome. Together these findings provide a clue to the genetic mechanism(s) underlying iNKT cell deficiency in NOD mice.




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