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Critical Role of NK Cells Rather Than V14⁺NKT Cells in Lipopolysaccharide-Induced Lethal Shock in Mice¹

Masashi Emoto^2,*, Mamiko Miyamoto^*, Izumi Yoshizawa^*, Yoshiko Emoto^*, Ulrich E. Schaible^*, Eiji Kita and Stefan H. E. Kaufmann^*

^* Department of Immunology, Max-Planck-Institute for Infection Biology, Berlin, Germany; and Department of Bacteriology, Nara Medical University, Nara, Japan

Although macrophages play a central role in the pathogenesis of septic shock, NK1⁺ cells have also been implicated. NK1⁺ cells comprise two major populations, namely NK cells and V14⁺NKT cells. To assess the relative contributions of these NK1⁺ cells to LPS-induced shock, we compared the susceptibility to LPS-induced shock of ₂-microglobulin (₂m)^-/- mice that are devoid of V14⁺NKT cells, but not NK cells, with that of wild-type (WT) mice. The results show that ₂m^-/- mice were more susceptible to LPS-induced shock than WT mice. Serum levels of IFN- following LPS challenge were significantly higher in ₂m^-/- mice, and endogenous IFN- neutralization or in vivo depletion of NK1⁺ cells rescued ₂m^-/- mice from lethal effects of LPS. Intracellular cytokine staining revealed that NK cells were major IFN- producers. The J281^-/- mice that are exclusively devoid of V14⁺NKT cells were slightly more susceptible to LPS-induced shock than heterozygous littermates. Hence, LPS-induced shock can be induced in the absence of V14⁺NKT cells and IFN- from NK cells is involved in this mechanism. In WT mice, hierarchic contribution of different cell populations appears likely.

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