| First Author | Dieli F | Year | 2000 |
| Journal | J Exp Med | Volume | 192 |
| Issue | 11 | Pages | 1645-52 |
| PubMed ID | 11104806 | Mgi Jnum | J:66081 |
| Mgi Id | MGI:1927950 | Doi | 10.1084/jem.192.11.1645 |
| Citation | Dieli F, et al. (2000) Resistance of natural killer T cell-deficient mice to systemic shwartzman reaction. J Exp Med 192(11):1645-52 |
| abstractText | 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 priming mechanism of the unique population of Valpha14 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. |
