There is growing evidence that T helper cell subsets (T(H)1 and T(H)2) can be differentially recruited to promote different types of inflammatory reactions. Murine T(H)1 but not T(H)2 cells are recruited through P-and E-selectin into inflamed tissues, where they induce delayed-type hypersensitivity reactions. The human eotaxin-receptor CCR3, originally described on eosinophils and basophils, was also found to be expressed by T(H)2 cells. An antibody to CCR3 was used to isolate T cells from peripheral blood that give rise to T(H)2-polarized cell lines and to identify T(H)2 cells derived from naive T cells in vitro. Eotaxin stimulated increases in intracellular calcium and chemotaxis of CCR3(+) T cells. The attraction of T(H)2 cells by eotaxin could represent a key mechanism in allergic reactions, because it promotes the allergen-driven production of interleukin-4 and interleukin-5 necessary to activate basophils and eosinophils.