In the present study, we investigated the role of resident cells in the neutrophil migration induced by ovalbumin (OVA) in immunized rats. OVA administration induced dose-dependent neutrophil migration, which was inhibited by pretreating the animals with dexamethasone, but not with indomethacin or BW 70C. Lymphocytes, but not macrophages or mast cells, obtained from sensitized animals and stimulated in vitro with OVA released a factor that induced neutrophil migration in vivo and in vitro. Both the release of this factor in vitro and the neutrophil migration induced in vivo were inhibited by dexamethasone, thus explaining the inhibitory effect of glucocorticoids on the neutrophil migration induced by OVA in immunized animals. Neither indomethacin nor BW 70C had any such effect. The fact that actinomycin D also inhibited the release of the factor from OVA-stimulated lymphocytes suggests that this substance is of a proteinaceous nature. The importance of lymphocytes for neutrophil recruitment in OVA-immunized rats was supported by the fact that homologous lymphocyte transfer into air pouches rendered these cavities responsive to OVA. Lymphocytes obtained from naive rats and stimulated with the lectins concanavalin A (Con A) or phytohaemagglutinin (PHA) were also able to release a factor that induced neutrophil migration in vivo. In vitro incubation of the supernatant from OVA-stimulated lymphocytes with antisera to interleukin-1 beta (IL-1 beta), IL-8 and tumour necrosis factor-alpha (TNF-alpha) did not inhibit the neutrophil chemotactic activity. These data suggest that IL-1 beta, IL-8 and TNF-alpha are not involved in the neutrophil chemotactic activity of the supernatant. Overall, these results indicate the importance of lymphocyte participation in neutrophil recruitment during inflammatory immune reaction, through the release of a neutrophil chemotactic factor different from IL-1 beta, IL-8 and TNF-alpha.