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Cutting Edge |
14-J281 NKT Cells Naturally Regulate Experimental Autoimmune Encephalomyelitis in Nonobese Diabetic Mice1
* Institut National de la Santé et de la Recherche Médicale, Unité 546, Hôpital Pitié-Salpetriere, and
Institut National de la Santé et de la Recherche Médicale, Unité 25, Hôpital Necker, and Unité 561, Hôpital Saint Vincent de Paul, Paris, France;
Institut National de la Santé et de la Recherche Médicale, Unité 563, Hôpital Purpan, Toulouse, France;
Department of Microbiology and Immunology, Howard Hughes Medical Institute, Vanderbilt University School of Medicine, Nashville, TN 37232; and
¶ Brain Research Institute, University of Vienna, Vienna, Austria
Although deficiencies in the NKT cell population have been
observed in multiple sclerosis and mouse strains susceptible to
experimental autoimmune encephalomyelitis (EAE), little is known about
the function of these cells in CNS autoimmunity. In this work we report
that TCR V
14-J281 transgenic nonobese diabetic mice, which are
enriched in CD1d-restricted NKT cells, are protected from EAE. The
protection is associated with a striking inhibition of Ag-specific
IFN-
production in the spleen, implying modulation of the
encephalitogenic Th1 response. This modulation is independent of IL-4
because IL-4-deficient V14-J281 mice are still protected against
EAE and independent of NKT cell-driven Th1 to Th2 deviation,
because no increased autoantigen-specific Th2 response was
observed in immunized V14-J281 transgenic mice. Our findings
indicate that enrichment and/or stimulation of CD1d-dependent NKT cells
may be used as a novel strategy to treat CNS
autoimmunity.
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