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© The Rockefeller University Press, 0022-1007/1999/10/963/ $5.00
The Journal of Experimental Medicine, Volume 190, Number 7, October 4, 1999 963-972

Original Article

A Defect in Interleukin 12–Induced Activation and Interferon {gamma} Secretion of Peripheral Natural Killer T Cells in Nonobese Diabetic Mice Suggests New Pathogenic Mechanisms for Insulin-Dependent Diabetes Mellitus

Marika Falconea, Brian Yeunga, Lee Tuckera, Enrique Rodrigueza, and Nora Sarvetnicka

a Department of Immunology, The Scripps Research Institute, La Jolla, California 92037
Department of Immunology, The Scripps Research Institute, 10550 North Torrey Pines Rd., La Jolla, CA 92037.858-784-9083858-784-9066

noras{at}scripps.edu

The function of natural killer T (NKT) cells in the immune system has yet to be determined. There is some evidence that their defect is associated with autoimmunity, but it is still unclear how they play a role in regulating the pathogenesis of T cell–mediated autoimmune diseases. It was originally proposed that NKT cells could control autoimmunity by shifting the cytokine profile of autoimmune T cells toward a protective T helper 2 cell (Th2) type. However, it is now clear that the major function of NKT cells in the immune system is not related to their interleukin (IL)-4 secretion. In fact, NKT cells mainly secrete interferon (IFN)-{gamma} and, activated in the presence of IL-12, acquire a strong inflammatory phenotype and cytotoxic function.

Key Words: natural killer T cells • interferon {gamma} • interleukin 4 • autoimmunity • regulatory cells

1used in this paper: EAE, experimental autoimmune encephalomyelitis; IDDM, insulin-dependent diabetes mellitus; NOD, nonobese diabetic

© 1999 The Rockefeller University Press


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