Abstract:
:Activation of invariant natural killer T (iNKT) cells by treatment with their α-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 (Jα18 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 Jα18 KO mice. Finally, we established that this natural anti-inflammatory function of iNKT cells depends on their IFN-γ 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.
journal_name
Eur J Immunoljournal_title
European journal of immunologyauthors
Bourgeois EA,Levescot A,Diem S,Chauvineau A,Bergès H,Milpied P,Lehuen A,Damotte D,Gombert JM,Schneider E,Girard JP,Gourdy P,Herbelin Adoi
10.1002/eji.201040647subject
Has Abstractpub_date
2011-02-01 00:00:00pages
299-305issue
2eissn
0014-2980issn
1521-4141journal_volume
41pub_type
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