Eosinophil IgE Receptors: Controversy and Consensus
During the past decade, considerable new information has been obtained about the function of the eosinophil and its role in human diseases. Presently, the eosinophil is recognized as a proinﬂammatory granulocyte implicated in protection against parasitic infection and believed to play an important role in allergic diseases, such as bronchial asthma, allergic rhinitis, and atopic dermatitis (1). The eosinophil is an important source of cytotoxic cationic proteins, such as major basic protein (MBP), eosinophil peroxidase, and eosinophil cationic protein, that have the potential of a two-edged sword: on the one hand, protecting the host against overwhelming helminth infections but, on the other hand, causing host tissue damage (2). Eosinophils can also induce inﬂammation by releasing lipid mediators, oxygen metabolites, and cytokines (2). Numerous studies have shown the association of eosinophils and various human parasitic and allergic diseases. For example, the most common cause of eosinophilia worldwide today is probably infection with helminths (3). Analyses of patients infected with Onchocerca volvulus have shown striking deposition of the eosinophil granule MBP around degenerating microﬁlaria (4). In allergic diseases, eosinophilic and lymphocytic inﬁltration in the epithelium and lamina propria of the airways have been consis-
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tent ﬁndings even in mild and stable asthma (5). Indeed, correlations have been observed between the number of inﬁltrating eosinophils and asthma disease severity (5). Pulmonary segmental allergen challenge in allergic individuals causes eosinophil recruitment into the airways; this is associated with the release of eosinophil granule proteins and an increase in vascular permeability (6,7). In spite of these strong associations among eosinophils, their cytotoxic granule proteins, and human diseases, the activation mechanism(s) of eosinophils in vivo has been largely unknown.