iNKT cells in inflamed peritoneum produced cytokines during the resolution of inflammation. (A) Day 0 or day 4 WT CD4 T cells were ex vivo–stimulated by PMA/ionomycin (Iono) or anti-CD3 and anti-CD28, and stained for intracellular IL-4 and IFN-γ. (B) Following stimulation with anti-CD3 and anti-CD28 for 24 hours, day 0 or day 4 CD4 T cells were gated into NKT (CD1d tetramer+ TCRβ +) and non-NKT (CD1d tetramer-TCRβ +) populations. Each population was assessed for intracellular IL-4 and IFN-γ. (C) IL-4, IL-13, and IFN-γ in supernatants after anti-CD3 and anti-CD28 stimulation were measured by ELISA. (D-G) Peritonitis was induced by sodium periodate injection in WT and Cd1d^−/− or Jα18^−/− mice. Inflammation was assessed by peritoneal cell counts (D, F). IL-4, IL-13, and IFN-γ in supernatants of Cd1d^−/− (E) or Jα18^−/− mice (G) day 4 CD4 T cells after anti-CD3 and anti-CD28 stimulation were measured by ELISA. (H) WT splenic NKT cells or PBS were adoptively transferred into WT or Jα18^−/− mice at 66 hours after sodium periodate injection. Peritoneal inflammation was scored by cell counts 30 hours later. (I) CD4 T cells from recipient mice in (H) were stimulated ex vivo for 48 hours, and IL-4 and IFN-γ were measured by ELISA. Data represent at least 2 independent experiments.