Resistance of natural killer T cell-deficient mice to systemic Shwartzman reaction

被引:55
作者
Dieli, F
Sireci, G
Russo, D
Taniguchi, M
Ivanyi, J
Fernandez, C
Troye-Blomberg, M
De Leo, G
Salerno, A
机构
[1] Natl Res Council, Inst Adv Diagnost Methodol, I-90134 Palermo, Italy
[2] Univ Palermo, Dept Biopathol, I-90134 Palermo, Italy
[3] Chiba Univ, Sch Med, Ctr Biomed Sci, Div Mol Immunol, Chiba 2608670, Japan
[4] Kings Coll London Guys Med & Dent Sch, London SE1 9RT, England
[5] Stockholm Univ, Dept Immunol, S-10691 Stockholm, Sweden
关键词
natural killer T cells; interferon gamma; interleukin; 12; lipopolysaccharide; Shwartzman reaction;
D O I
10.1084/jem.192.11.1645
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The generalized Shwartzman reaction in mice which had been primed and challenged with lipopolysaccharide (LPS) depends on interleukin (IL)-12-induced interferon (IFN)-gamma production at the priming stage. We examined the involvement in the printing mechanism of the unique population of V alpha 14, natural killer T (NKT) cells because they promptly produce IFN-gamma 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-gamma production, because injection of recombinant mouse IFN-gamma, 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.
引用
收藏
页码:1645 / 1651
页数:7
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