期刊
EUROPEAN JOURNAL OF IMMUNOLOGY
卷 41, 期 2, 页码 299-305出版社
WILEY
DOI: 10.1002/eji.201040647
关键词
IL-33; Inflammation; iNKT cells; Innate cells
类别
资金
- CNRS
- INSERM
- Universites Paris V Descartes et Paris-Sud XI
- Chancellerie des Universites de Paris (Legs Poix)
- Ministere de l'Education Nationale de la Recherche et de la Technologie
- Nouvelles Recherches Medicales - Vaincre le cancer
Activation of invariant natural killer T (iNKT) cells by treatment with their alpha-galactosyl ceramide ligand provides therapeutic benefits in several immune inflammatory settings. Given the artificial nature of this stimulation, the natural regulatory functions of iNKT remain uncertain. Addressing this issue in a mouse model of innate-cell-driven lung inflammation induced by the cytokine/alarmin IL-33 that targets iNKT cells, we found that eosinophil and neutrophil recruitment was markedly increased in treated iNKT cell-deficient (J alpha 18 KO) mice, as was the local production of eotaxin and keratinocyte chemoattractant chemokines. By contrast, lung inflammation decreased after adoptive transfer of iNKT cells, which restored the WT inflammatory response in J alpha 18 KO mice. Finally, we established that this natural anti-inflammatory function of iNKT cells depends on their IFN-gamma production and on endogenous IL-12. Our study provides the first evidence of a protective role of iNKT cells during lung inflammation that does not require pharmacological TCR engagement.
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