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24JQ Invariant TCR Chain in the Lesions of Multiple Sclerosis and Chronic Inflammatory Demyelinating Polyneuropathy1
*
Department of Demyelinating Disease and Aging, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Ogawahigashi, Kodaira, Tokyo, Japan;
NeuroResource, Institute of Neurology, London, United Kingdom;
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
24+ NK T cells are a unique subset of
lymphocytes expressing the V24JQ 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 V24JQ 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
V24JQ NK T cells, but multiple sclerosis lesions only rarely
expressed the V24JQ 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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