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Division of Developmental Immunology, La Jolla Institute for Allergy and Immunology, La Jolla, CA 92037; and Division of Biology, University of California San Diego, La Jolla, CA 92093
NKT cells are thought of as a bridge between innate and adaptive immunity. In this study, we demonstrate that mouse NKT cells are activated in response to Escherichia coli LPS, and produce IFN-
, but not IL-4, although activation through their TCR typically induces both IL-4 and IFN- production. IFN- production by NKT cells is dependent on LPS-induced IL-12 and IL-18 from APC. LPS induced IFN- production by NKT cells does not require CD1d-mediated presentation of an endogenous Ag and exposure to a combination of IL-12 and IL-18 is sufficient to activate them. In mice that are deficient for NKT cells, innate immune cells are activated less efficiently in response to LPS, resulting in the reduced production of TNF and IFN-. We propose that in addition to acting as a bridge to adaptive immunity, NKT cells act as an early amplification step in the innate immune response and that the rapid and complete initiation of this innate response depends on the early production of IFN- by NKT cells.
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 Grant R37 AI71922 from the National Institutes of Health (to M.K.).
2 Address correspondence and reprint requests to Dr. Mitchell Kronenberg, La Jolla Institute for Allergy and Immunology, 9420 Athena Circle, La Jolla, CA 92037. E-mail address: mitch{at}liai.org
3 Abbreviations used in this paper: iNKT, invariant NKT; GSL, glycosphingolipid; 
GalCer, -galactosylceramide; rm, recombinant murine; ICCS, intracellular cytokine staining; DC, dendritic cell; Tg, transgenic; BM, bone marrow.
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