Brief Definitive Report

Resistance of Natural Killer T Cell-deficient Mice to Systemic Shwartzman Reaction

Correspondence to: Alfredo Salerno, Institute of Advanced Diagnostic Methodologies, National Research Council, Corso Tukory, 211, 90134 Palermo, Italy. Tel:39-091-655-5903 Fax:39-091-655-5901 E-mail:asalerno{at}unipa.it.

The generalized Shwartzman reaction in mice which had been primed and challenged with lipopolysaccharide (LPS) depends on interleukin (IL)-12–induced interferon (IFN)- production at the priming stage. We examined the involvement in the priming mechanism of the unique population of V14 natural killer T (NKT) cells because they promptly produce IFN- after IL-12 stimulation. We report here that LPS- or IL-12–primed NKT cell genetically deficient mice were found to be resistant to LPS-elicited mortality. This outcome can be attributed to the reduction of IFN- production, because injection of recombinant mouse IFN-, but not injection of IL-12, effectively primed the NKT cell–deficient mice. However, priming with high doses of LPS caused mortality of severe combined immunodeficiency, NKT cell–deficient, and CD1-deficient mice, indicating a major contribution of NKT cells to the Shwartzman reaction elicited by low doses of LPS, whereas at higher doses of LPS NK cells play a prominent role. These results suggest that the numerically small NKT cell population of normal mice apparently plays a mandatory role in the priming stage of the generalized Shwartzman reaction.

Key Words: natural killer T cells, interferon , interleukin 12, lipopolysaccharide, Shwartzman reaction

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