[Eosinophils in immediate allergic reactions].

Large numbers of eosinophils infiltrate the tissue in patients with various allergic disorders including asthma. Many appear to be degranulated to release mediators, granular proteins and superoxides, and are thereby considered to play an important role in tissue damage. Human eosinophils possess membrane receptors for IgE (Fc epsilon R II) and IgE-dependent eosinophil activation and following degranulation may be involved in immediate-type allergic reactions. Several lines of experimental evidence also suggest other eosinophil activation mechanisms by the stimulation of platelet-activating factor (PAF), leukotriene B4 and cytokines such as interleukin 5. Among these, PAF is a potent chemoattractant for eosinophils and is also capable of inducing activation such as a change from normodense into hypodense eosinophils. In animal models of allergic asthma, a specific PAF antagonist blocked eosinophil infiltration which was observed 6 hr after antigen challenge. However, another peak of tissue eosinophilia seen 24 hr after the challenge was not inhibited by PAF antagonist but was abolished by cyclosporin A, a T cell suppressant. These data suggested that PAF and T cell-derived factor(s) may be important in the pathogenesis of tissue eosinophilia observed in allergic reactions.