Invariant natural killer T (iNKT) cells are a subset of innate T cells that recognize glycolipids presented on CD1d molecules. These cells are crucial for protection against bacterial infections, including respiratory Streptococcous pneumoniae infection. The lung harbors a resident population of iNKT cells, although these cells have been implicated to play a role in many pulmonary disease models, little is known about their behavior, localization, and function. Using lung intravital microscopy, we examined the behavior and mechanism of pulmonary iNKT cell activation in response to the specific iNKT cell ligand a-galactosylceramide or S. pneumoniae infection. In naive mice, the major fraction of iNKT cells resided in the vasculature, but a small critical population resided in the extravascular space.  Administration of either a-GalCer or S. pneumoniae into the airways induced CD1d-dependent rapid recruitment of neutrophils out of the vasculature. These neutrophils guided iNKT cells from the lung vasculature via CCL17. Depletion of monocyte-derived DCs abrogated both the neutrophil and subsequent iNKT cell extravasation and activation. Moreover, impairing pulmonary iNKT cell extravasation by blocking CCL17 increased susceptibility to S. pneumoniae infection, suggesting a critical role for specifically pulmonary iNKT cell extravasation and activation in host defense.