Mechanisms of eosinophilia in the pathogenesis of hypereosinophilic disorders.
The increased numbers of activated eosinophils in the blood and tissues that typically accompany hypereosinophilic disorders result from a variety of mechanisms. Exciting advances in translating discoveries achieved from mouse models and molecular strategies to the clinic have led to a flurry of new therapeutics specifically designed to target eosinophil-associated diseases. So far, this form of hypothesis testing in humans in vivo through pharmacology generally has supported the paradigms generated in vitro and in animal models, raising hopes that a spectrum of novel therapies soon may become available to help those who have eosinophil-associated diseases.
Ackerman
Steven J
SJ
Department of Biochemistry and Molecular Genetics (M/C 669), Molecular Biology Research Building, Rm. 2074, 900 S. Ashland Avenue, The University of Illinois at Chicago College of Medicine, Chicago, IL 60607, USA.
Bochner
Bruce S
BS
D000818:Animals; D015550:Cell Degranulation; D002631:Chemotactic Factors, Eosinophil / Q000378:metabolism; D016207:Cytokines / Q000276:immunology / Q000378:metabolism*; D047091:Eosinophil Granule Proteins / Q000276:immunology / Q000378:metabolism*; D004804:Eosinophils / Q000276:immunology* / Q000502:physiology*; D006801:Humans; D017681:Hypereosinophilic Syndrome / Q000097:blood / Q000276:immunology / Q000503:physiopathology*; D018836:Inflammation Mediators / Q000276:immunology / Q000378:metabolism*; D019891:Leukopoiesis
D002631:Chemotactic Factors, Eosinophil; D016207:Cytokines; D047091:Eosinophil Granule Proteins; D018836:Inflammation Mediators