Abstract 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 Jα18−/− mice contained few Ly6G+CD11b+ granulocytes, whereas levels in B6 mice were greater and were increased further by α-galactosyl ceramide. IFN-γ and MIP-1α production in the lungs was greater in B6 than CD1d−/− mice. Adoptive transfer of wild type (WT) but not IFN-γ–, MIP-1α–, or FcγR-deficient NKT cells into CD1d−/− mice caused recruitment of inflammatory cells to the lungs. Moreover, adoptive transfer of IFN-γR–deficient NKT cells enhanced MIP-1α production and cell recruitment in the lungs of CD1d−/− or CD1d−/−IFN-γ−/− mice, but to a lesser extent than WT NKT cells. This suggests that IFN-γ–producing NKT cells enhance MIP-1α production in both an autocrine and a paracrine manner. IFN-γ–deficient NKT cells induced less IL-1β and TNF-α production by alveolar macrophages and dendritic cells in CD1d−/− mice than did WT NKT cells. Taken together, these data suggest that CD1d-restricted IFN-γ–producing NKT cells promote IC-ALI by producing MIP-1α and enhancing proinflammatory cytokine production by alveolar macrophages and dendritic cells.