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

doi:10.1084/jem.192.11.1645

Published online 4 December 2000.

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© The Rockefeller University Press, 0022-1007/2000/12/1645/ $5.00
The Journal of Experimental Medicine, Volume 192, Number 11, December 4, 2000 1645-1652

Brief Definitive Report

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

Francesco Dieli^a, Guido Sireci^a, Domenica Russo^b, Masaru Taniguchi^c, Juraj Ivanyi^d, Carmen Fernandez^e, Marita Troye-Blomberg^e, Giacomo De Leo^a, and Alfredo Salerno^a,b
^a Department of Biopathology, University of Palermo,
^b Institute for Advanced Diagnostic Methodologies, National Research Council, 90134 Palermo, Italy
^c Division of Molecular Immunology, Center for Biomedical Science, School of Medicine, Chiba University, Chiba 260-8670, Japan
^d King's College London at Guy's Medical and Dental School, London SE1 9RT, United Kingdom
^e Department of Immunology, Stockholm University, S-106 91 Stockholm, Sweden

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 primedand challenged with lipopolysaccharide (LPS) depends on interleukin(IL)-12–induced interferon (IFN)- ${gamma}$ production at the primingstage. We examined the involvement in the priming mechanismof the unique population of V ${alpha}$ 14 natural killer T (NKT) cellsbecause they promptly produce IFN- ${gamma}$ after IL-12 stimulation.We report here that LPS- or IL-12–primed NKT cell geneticallydeficient mice were found to be resistant to LPS-elicited mortality.This outcome can be attributed to the reduction of IFN- ${gamma}$ production,because injection of recombinant mouse IFN- ${gamma}$ , but not injectionof IL-12, effectively primed the NKT cell–deficient mice.However, priming with high doses of LPS caused mortality ofsevere combined immunodeficiency, NKT cell–deficient,and CD1-deficient mice, indicating a major contribution of NKTcells 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 populationof normal mice apparently plays a mandatory role in the primingstage of the generalized Shwartzman reaction.

Key Words: natural killer T cells, interferon ${gamma}$ , interleukin 12, lipopolysaccharide,Shwartzman reaction

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