Expression of chemokine receptors on T helper 2 cells and eosinophils has been postulated
to be the mechanism by which these cells are selectively recruited to the lung during allergic
inflammatory reactions. Mouse models have provided evidence to show that blocking the
ligands for these receptors is successful in abrogating the pathophysiological effects of
allergen challenge. However, recent studies describing the effect of genetic deletions of
these chemokine receptors have not confirmed the results obtained with ligand knockouts or …