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* Department of Microbiology and Immunology, and
Department of Medicine, Albert Einstein College of Medicine, Bronx, NY 10461;
Laboratory of Bacterial Pathogenesis and Immunology, The Rockefeller University, New York, NY 10021;
Institute of Hansen’s Disease, Catholic University, Seoul, South Korea;
¶ School of Biosciences, University of Birmingham, Edgbaston, Birmingham, United Kingdom;
|| Edward Hines, Jr. Veterans Affairs Hospital, Hines, IL 60141; and
# Division of Dermatology,
** Department of Microbiology, Immunology, and Molecular Genetics, David Geffen School of Medicine, University of California, Los Angeles, CA 90095
CD1d-restricted NKT cells expressing invariant TCR 
-chains (iNKT cells) produce both proinflammatory and anti-inflammatory cytokines rapidly upon activation, and are believed to play an important role in both host defense and immunoregulation. To address the potential implications of iNKT cell responses for infectious or inflammatory diseases of the nervous system, we investigated the expression of CD1d in human peripheral nerve. We found that CD1d was expressed on the surface of Schwann cells in situ and on primary or immortalized Schwann cell lines in culture. Schwann cells activated iNKT cells in a CD1d-dependent manner in the presence of -galactosylceramide. Surprisingly, the cytokine production of iNKT cells stimulated by -galactosylceramide presented by CD1d+ Schwann cells showed a predominance of Th2-associated cytokines such as IL-5 and IL-13 with a marked deficiency of proinflammatory Th1 cytokines such as IFN-
or TNF-. Our findings suggest a mechanism by which iNKT cells may restrain inflammatory responses in peripheral nerves, and raise the possibility that the expression of CD1d by Schwann cells could be relevant in the pathogenesis of infectious and inflammatory diseases of the peripheral nervous system.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 This work was supported by National Institutes of Health Grants AI 45816 and NS 45187 (to A.R.), Grant AR 40312 (to R.L.M.), and Grants AI 45889, AI 51391, and AI 064424 (to S.A.P.). This work was also supported by Grants G9901077 and G0400421 from the Medical Research Council and Grant 072021/Z/03/Z from the Wellcome Trust (to G.S.B.). G.S.B. is a Lister-Jenner Research Fellow. Flow cytometry studies were supported by funding to the Center for AIDS Research (Grant AI051519) and the Cancer Center (Grant CA 133330) at the Albert Einstein College of Medicine.
2 Address correspondence and reprint requests to Dr. Steven A. Porcelli, Department of Microbiology and Immunology, Forchheimer Building, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461.
3 Abbreviations used in this paper: iNKT, invariant NKT; GalCer, -galactosylceramide; DC, dendritic cell; MPNST, malignant peripheral nerve sheath tumor.
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