Umetsu D T, DeKruyff R H
Department of Pediatrics, Stanford University, California 94305-5119, USA.
Proc Soc Exp Biol Med. 1997 May;215(1):11-20. doi: 10.3181/00379727-215-44109.
Our understanding of the molecular and genetic etiologies of allergic disorders, which affect 20%-30% of the general population, has greatly improved over the past several years. Previously, research focused on examination of immediate hypersensitivity reactions, initiated by the cross-linking of IgE molecules on the surface of mast cells/basophils, resulting in the release of a host of mediators, which cause symptoms typified by acute anaphylaxis. Although there has been substantial progress in understanding the molecular biology of mast cell and basophil activation and of the regulation of IgE synthesis, recent studies have shifted attention to the cellular and molecular mechanisms that cause a broader allergic inflammatory response and underlie the more chronic and severe symptoms of allergy and asthma. In this report, we will review a substantial body of recent experimental work that has provided the basis for our new understanding of the allergic inflammatory response and the pathogenesis of allergic diseases. We will describe the recent progress in defining the immunological basis for allergic disease, and how subsets of helper CD4+ T cells secreting a specific array of cytokines (Th2 cytokines) regulate/cause allergic inflammation. We will review the cell biology of Th2 cells, the role of Th2 cells in allergic disease, and biological, genetic, and therapeutic mechanisms that influence the differentiation of CD4+ T cells and enhance or suppress cytokine synthesis in Th2 cells. These mechanisms control the expression of allergic diseases, which occur in some but not all individuals following environmental exposure to allergens.
过敏症影响着20%-30%的普通人群，在过去几年里，我们对其分子和遗传病因的理解有了很大提高。以前，研究主要集中在检查速发型超敏反应，这种反应由肥大细胞/嗜碱性粒细胞表面的IgE分子交联引发，导致大量介质释放，从而引起以急性过敏反应为典型的症状。尽管在理解肥大细胞和嗜碱性粒细胞活化的分子生物学以及IgE合成的调节方面取得了重大进展，但最近的研究已将注意力转移到引发更广泛的过敏性炎症反应并构成过敏和哮喘更慢性、更严重症状基础的细胞和分子机制上。在本报告中，我们将回顾大量近期的实验工作，这些工作为我们对过敏性炎症反应和过敏性疾病发病机制的新理解提供了基础。我们将描述在确定过敏性疾病的免疫学基础方面的最新进展，以及分泌特定细胞因子阵列（Th2细胞因子）的辅助性CD4+ T细胞亚群如何调节/引发过敏性炎症。我们将回顾Th2细胞的细胞生物学、Th2细胞在过敏性疾病中的作用，以及影响CD4+ T细胞分化并增强或抑制Th2细胞中细胞因子合成的生物学、遗传和治疗机制。这些机制控制着过敏性疾病的表达，过敏性疾病在一些但不是所有个体接触环境过敏原后发生。
