Study on a novel mechanism by which IgE/FcεRI mediates chronic allergic inflammation

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The recruitment of basophils into the sites of allergic inflammation is often observed. However, no definitive evidence has been provided that basophils are crucially involved in the pathogenesis of chronic allergic disorders. Basophils represent less than 1% of peripheral blood leukocytes. and have often been considered as minor and possibly redundant "circulating mast cells". In this study, we have demonstrated that basophils play an important and non-redundant role and are responsible for the development of IgE-mediated chronic allergic inflammation, independently of T cells and mast cells. A single subcutaneous injection of multivalent antigens elicited not only immediate- and late-phase ear swelling but also delayed-onset ear swelling with massive eosinophil infiltration in mice sensitized with antigen-specific IgE and IgE transgenic mice. Mast cells were essential for the immediate- and late-phase ear swelling but dispensable for the delayed one. T cells were also dispensable for the latter. The delayed-onset allergic inflammation was not developed in FcεRI-deficient mice, but it was restored in these mice by transferring FcεRI-expressing basophils from normal mice. These findings indicate a novel mechanism of development of chronic allergic inflammation that is induced by basophils through the-interaction of antigen, IgE, and FcεRI. The present study implies that basophils and their products could be good targets to treat this type of chronic allergic inflammation.