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The Journal of Immunology, 2000, 164: 4375-4381.
Copyright © 2000 by The American Association of Immunologists

Differential Expression of NK T Cell V{alpha}24J{alpha}Q Invariant TCR Chain in the Lesions of Multiple Sclerosis and Chronic Inflammatory Demyelinating Polyneuropathy1

Zsolt Illés2,*, Takayuki Kondo2,*, Jia Newcombe{dagger}, Nobuyuki Oka{ddagger}, Takeshi Tabira* and Takashi Yamamura3,*

* Department of Demyelinating Disease and Aging, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Ogawahigashi, Kodaira, Tokyo, Japan; {dagger} NeuroResource, Institute of Neurology, London, United Kingdom; {ddagger} Department of Neurology, Faculty of Medicine, Kyoto University, Kyoto, Japan; and § Department of Immunology, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo, Japan

Human V{alpha}24+ NK T cells are a unique subset of lymphocytes expressing the V{alpha}24J{alpha}Q invariant TCR chain. Because they can rapidly produce large amounts of regulatory cytokines, a reduction of NK T cells may lead to the development of certain autoimmune diseases. Using a single-strand conformation polymorphism method, we demonstrate that a great reduction of V{alpha}24J{alpha}Q NK T cells in the peripheral blood is an immunological hallmark of multiple sclerosis, whereas it is not appreciable in other autoimmune/inflammatory diseases such as chronic inflammatory demyelinating polyneuropathy. The chronic inflammatory demyelinating polyneuropathy lesions were often found to be infiltrated with V{alpha}24J{alpha}Q NK T cells, but multiple sclerosis lesions only rarely expressed the V{alpha}24J{alpha}Q TCR. It is therefore possible that the extent of NK T cell alteration may be a critical factor which would define the clinical and pathological features of autoimmune disease. Although the mechanism underlying the NK T cell deletion remains largely unclear, a remarkable contrast between the CNS and peripheral nervous system diseases allows us to speculate a role of tissue-specific elements such as the level of CD1d expression or differences in the CD1d-bound glycolipid.




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