Abstract

The allergic inflammatory response is composed of two main phases--the early and the late. The early phase initiates when an allergen activates the tissue resident mast cell, triggering the release of a variety of granule-stored and newly formed mediators. As the inflammatory response progresses, blood borne inflammatory cells--in particular, eosinophils--are recruited into the inflamed tissue. Eosinophil activation and consequent release and production of several pro-inflammatory mediators results in the late phase reaction. A chronic allergic inflammation always features prominent tissue eosinophilia. In this review, we will discuss the possible channels of communication, both soluble and physical, between mast cells and eosinophils that can occur in the late and chronic stages of allergy. Such interactions, that we have termed "the allergic effector unit", may modulate the severity and/or duration of the allergic inflammatory reaction.

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