| First Author | Kim JH | Year | 2011 |
| Journal | J Immunol | Volume | 186 |
| Issue | 3 | Pages | 1432-41 |
| PubMed ID | 21191075 | Mgi Jnum | J:168903 |
| Mgi Id | MGI:4939286 | Doi | 10.4049/jimmunol.1003140 |
| Citation | Kim JH, et al. (2011) CD1d-restricted IFN-gamma-secreting NKT cells promote immune complex-induced acute lung injury by regulating macrophage-inflammatory protein-1alpha production and activation of macrophages and dendritic cells. J Immunol 186(3):1432-41 |
| abstractText | Immune complex-induced acute lung injury (IC-ALI) has been implicated in various pulmonary disease states. However, the role of NKT cells in IC-ALI remains unknown. Therefore, we explored NKT cell functions in IC-ALI using chicken egg albumin and anti-chicken egg albumin IgG. The bronchoalveolar lavage fluid of CD1d(-/-) and Jalpha18(-/-) mice contained few Ly6G(+)CD11b(+) granulocytes, whereas levels in B6 mice were greater and were increased further by alpha-galactosyl ceramide. IFN-gamma and MIP-1alpha production in the lungs was greater in B6 than CD1d(-/-) mice. Adoptive transfer of wild type (WT) but not IFN-gamma-, MIP-1alpha-, or FcgammaR-deficient NKT cells into CD1d(-/-) mice caused recruitment of inflammatory cells to the lungs. Moreover, adoptive transfer of IFN-gammaR-deficient NKT cells enhanced MIP-1alpha production and cell recruitment in the lungs of CD1d(-/-) or CD1d(-/-)IFN-gamma(-/-) mice, but to a lesser extent than WT NKT cells. This suggests that IFN-gamma-producing NKT cells enhance MIP-1alpha production in both an autocrine and a paracrine manner. IFN-gamma-deficient NKT cells induced less IL-1beta and TNF-alpha production by alveolar macrophages and dendritic cells in CD1d(-/-) mice than did WT NKT cells. Taken together, these data suggest that CD1d-restricted IFN-gamma-producing NKT cells promote IC-ALI by producing MIP-1alpha and enhancing proinflammatory cytokine production by alveolar macrophages and dendritic cells. |
