Following exposure with TSLP and antigen in the lungs, both CD11cIM and DC uptake antigen. Antigen-bearing DC migrate into the LdLN, whereas CD11cIM remain in the lungs. In the LdLN, Th2 that are generated by DC play a limited role for the acute inflammation in the lungs. In contrast, in the lungs, direct TSLP/TSLPR signal increases the potency of CD11cIM as APC for promoting differentiation of naïve CD4 T cells into primary effector Th2 cells and subsequent acute eosinophilic airway inflammation.