Garn Holger, Renz Harald
Department of Clinical Chemistry and Molecular Diagnostics, Medical Faculty, Philipps University of Marburg, Biomedical Research Center, Hans-Meerwein-Str. 2, 35043 Marburg, Germany.
Immunobiology. 2007;212(6):441-52. doi: 10.1016/j.imbio.2007.03.006. Epub 2007 Apr 30.
Allergic diseases are inflammatory disorders that develop on the basis of complex gene-environment interactions. The prevalence of allergies is steadily increasing and seems to be associated with modern lifestyle. Therefore, it was hypothesized that high living standards and hygienic conditions are correlated with an increased risk for the development of an allergic disease. This so-called "hygiene hypothesis" states that due to reduced exposure to microbial components, the proposed allergy-preventing potential of these factors is no more present in sufficient qualities and/or quantities, which leads to an imbalance of the immune system with a predisposition to the development of allergic disorders. Meanwhile, several epidemiological studies were conducted supporting this concept and generating novel ideas for the underlying mechanisms that were then followed up by use of well-defined animal models and human studies. The current view of cellular and molecular mechanisms responsible for these phenomena includes changes in the fine balancing of T helper cell 1 (Th1), Th2 and regulatory T cell (Treg) responses which are triggered by altered or missing innate immune cell activation. In fact, proper activation of cells of the innate immune system via their so-called pattern recognition receptors has been demonstrated to play a crucial role in early shaping of the immune system and suppression of the development of Th2-driven allergic immune responses. These processes start already in utero and prenatal as well as early postnatal developmental stages seem to represent a certain "window of opportunity" for allergy-preventing environmental influences.
过敏性疾病是基于复杂的基因-环境相互作用而发生的炎症性疾病。过敏症的患病率正在稳步上升，似乎与现代生活方式有关。因此，有人提出假说，高生活水平和卫生条件与过敏性疾病发生风险的增加相关。这个所谓的“卫生假说”指出，由于接触微生物成分减少，这些因素原本所具有的预防过敏的潜力不再以足够的质量和/或数量存在，这导致免疫系统失衡，易患过敏性疾病。与此同时，开展了多项流行病学研究来支持这一概念，并为潜在机制提出了新观点，随后通过使用明确的动物模型和人体研究对这些机制进行了跟进。目前对导致这些现象的细胞和分子机制的看法包括辅助性T细胞1（Th1）、Th2和调节性T细胞（Treg）反应的精细平衡发生变化，这些变化是由先天性免疫细胞激活的改变或缺失所触发的。事实上，通过所谓的模式识别受体对先天性免疫系统细胞进行适当激活已被证明在免疫系统的早期塑造以及抑制Th2驱动的过敏性免疫反应的发展中起着关键作用。这些过程在子宫内就已开始，产前以及出生后的早期发育阶段似乎代表了预防过敏的环境影响的特定“机会窗口”。
