Abstract
The regulation of tissue eosinophilia in allergic skin lesions were examined using chemotactic chamber assay. Tissue eosinophilia manifested two phases: early phase peaking at 6hr and delayed phase at 24hr. More potent delayed phase was mediated by two different eosinophil chemotactic factors, delayed ECF-a and b. Delayed ECF-a was shown to be a lymphokine produced by T lymphocytes through antigenic or mitogenic stimulation, whereas delayed ECF-b was produced by reaction with anti-hapten IgG1 antibody. The Delayed eosinophilia was suppressed completly when animals were treated with complete Freund's adjuvant. This suppression was due to the production of eosinophil-directed chemotactic inhibitory factor (ECIF) which selectively inhibit the chemotactic response of eosinophils to delayed ECF-a but not to delayed ECF-b.
On the other hands, tissue eosinophilia was markedly potentiated when animals were treated with alum hydroxy gel or Bordetella pertussis vaccine. This potentiation was ascribed to the potentiation of delayed ECF-a production by T lymphocytes. Macrophage products, named ECF-potentiating factors, could potentiate ECF-production but not macrophage chemotactic factor production. These results suggested that tissue eosinophilia, especially by a lymphokine (delayed ECF-a), is regulated by a lymphokine (ECIF) selectively, and that macrophage products are involved in the ECF production.
