Ackerman Steven J, Bochner Bruce S
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.
Immunol Allergy Clin North Am. 2007 Aug;27(3):357-75. doi: 10.1016/j.iac.2007.07.004.
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.
嗜酸性粒细胞增多性疾病通常伴随血液和组织中活化嗜酸性粒细胞数量增加，这是由多种机制导致的。从小鼠模型和分子策略所取得的发现向临床转化方面令人兴奋的进展，催生了一系列专门针对嗜酸性粒细胞相关疾病设计的新疗法。到目前为止，这种通过药理学在人体进行体内假设检验的形式总体上支持了在体外和动物模型中产生的范例，这让人们燃起希望，即很快可能会有一系列新疗法可供患有嗜酸性粒细胞相关疾病的患者使用。
