Modulation of eosinophil effector functions: the potential role of monoclonal antibodies and chemokine receptor antagonists.

Abstract

Increased numbers of eosinophils in the peripheral blood and inflammatory tissue are characteristic features of allergic diseases such as allergic asthma, rhinoconjunctivitis, and atopic dermatitis. Tissue damage and propagation of inflammation is thought to be mediated by the interaction among Th2-like T cells, antigen-presenting cells, and eosinophils. In this process eosinophils are activated by several inflammatory mediators, leading to the influx of eosinophils at sites of inflammation and to tissue damage by the release of reactive oxygen species and toxic granule proteins. Therefore, agents that would be able to inhibit or antagonize mediator-induced eosinophil activation seem to be possibilities as new therapeutic strategies. In this review we will focus on the modulation of human eosinophil effector functions by monoclonal antibodies and chemokine receptor antagonists. We will discuss whether modulation of eosinophil effector functions might be successful as a possible future strategy of diseases that are accompanied by activated eosinophils. Even when these compounds show antagonistic effects on human eosinophils, in vitro future studies will be necessary to investigate whether chemokine receptor antagonists and monoclonal antibodies are suitable in vivo in an animal model prior to studies in humans.