CD4+ Th1 and Th2 cells are critical mediators of inflammatory diseases. In
the lung, Th1-dominated responses are associated with the presence of a lar
ge number of macrophages and neutrophils. By contrast, eosinophilic inflamm
ation associated with mucus hypersecretion is dependent on the presence of
Th2 cells. Here we review the traffic signals that enable the differential
remitment of Th1 and Th2 cells for the inflammatory response in the lung.