Mice sensitized for a Th2 response to Leishmania LACK antigen developed allergic airway inflammation upon exposure to LACK aerosol. Using multimers of I-A^d molecules bound to a LACK peptide as probes, we tracked the migration of LACK-specific Th2 cells to the airways. Elevated numbers of LACK-specific Th2 cells remained in the airways for 5 weeks after the last aerosol. Substantial numbers of DC presenting LACK peptides were found in the airways, but not in other compartments, for up to 8 weeks after antigen exposure. These LACK-presenting airway DC expressed CD11c and CD11b as well as high levels of surface molecules involved in uptake and costimulation. Taken together, our results may explain the chronic Th2 airway inflammation characteristic of allergic asthma.