Department of Medicine, Section of Allergy and Immunology, University of California at San Diego, Calif, USA.
J Allergy Clin Immunol. 2011 Mar;127(3):689-95. doi: 10.1016/j.jaci.2011.01.027.
2010 was marked by rapid progress in our understanding of the cellular and molecular mechanisms involved in the pathogenesis of allergic inflammation and asthma. Studies published in the Journal of Allergy and Clinical Immunology described advances in our knowledge of cells associated with allergic inflammation (mast cells, eosinophils, dendritic cells, and T cells), as well as IgE, cytokines, receptors, signaling molecules, and pathways. Studies used animal models, as well as human cells and tissues, to advance our understanding of mechanisms of asthma, eosinophilic esophagitis, food allergy, anaphylaxis and immediate hypersensitivity, mast cells and their disorders, atopic dermatitis, nasal polyposis, and hypereosinophilic syndromes. Additional studies provided novel information about the induction and regulation of allergic inflammation and the genetic contribution to allergic inflammation. Critical features of these studies and their potential effects on human atopic disorders are summarized here.
2010 年，我们在理解过敏炎症和哮喘发病机制中的细胞和分子机制方面取得了快速进展。发表在《过敏与临床免疫学杂志》上的研究描述了我们对与过敏炎症相关的细胞（肥大细胞、嗜酸性粒细胞、树突状细胞和 T 细胞）以及 IgE、细胞因子、受体、信号分子和途径的认识的进展。这些研究使用动物模型以及人类细胞和组织，增进了我们对哮喘、嗜酸性食管炎、食物过敏、过敏反应和速发型超敏反应、肥大细胞及其疾病、特应性皮炎、鼻息肉和高嗜酸性粒细胞综合征的机制的理解。其他研究提供了关于过敏炎症的诱导和调节以及遗传对过敏炎症的贡献的新信息。本文总结了这些研究的关键特征及其对人类特应性疾病的潜在影响。
