[Clinical relevance on the inhibition of eosinophil functions--a review with special reference to eosinophilopietic cytokines].
Theoretical strategies for the inhibition of eosinophil function could be multistep. The pivotal role of GM-CSF, IL-3 or IL-5 in up-regulating eosinophil number and function might be specific targeting of therapy. Drugs attenuating T cells which generate those cytokines would induce a clinical remission by reducing the generation of a regulatory cytokine. Alternatively, therapies may be attained by blocking cytokine receptor binding at the level of the target stem cell or the mature eosinophil. Inhibition of eosinophil recruitment from peripheral blood to inflammatory tissue compartment will also be the site of therapy by inhibiting adhesion molecule function. Direct inhibition of chemical mediator release such as cytotoxic granular basic proteins, leukotrienes, PAF and superoxides from activated eosinophil would be another target for developing new drugs.
Department of Internal Medicine, Toho University School of Medicine, Sakura Hospital.
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Tomioka
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Kagami
D000818:Animals; D002454:Cell Differentiation; D002455:Cell Division; D016207:Cytokines / Q000378:metabolism / Q000502:physiology*; D004804:Eosinophils / Q000166:cytology / Q000502:physiology*; D010972:Platelet Activating Factor / Q000378:metabolism; D013481:Superoxides / Q000378:metabolism; D013601:T-Lymphocytes / Q000378:metabolism; D015854:Up-Regulation
D016207:Cytokines; D010972:Platelet Activating Factor; D013481:Superoxides