Burgio G R, Nespoli L, Ugazio A G
Eur J Pediatr. 1978 Dec 1;129(4):221-9. doi: 10.1007/BF00441353.
Despite impressive recent advances in the understanding of the chemical and cellular bases of the reaginic response, the pathogenesis of atopic diseases still remains a matter of speculation. The frequent finding of atopic diseases in some primary immunodeficiencies such as selective IgA deficiency and the Wiskott-Aldrich syndrome offers a unique opportunity for studying the immune mechanisms underlying the genesis of atopy. Recent studies in subjects with selective IgA deficiency have challenged the well known hypothesis that atopy is the result of defective "immune exclusion" by the secretory immune system. A number of immunological features found in the primary immunodeficiencies associated with atopic disorders suggest that defective homeostatic mechanisms regulating reaginic responses may play a major role in the pathogenesis of atopy. A thorough analysis of these disease combinations may help to generate new working hypotheses concerning the immune pathogenesis of atopic diseases.
尽管最近在对反应素反应的化学和细胞基础的理解方面取得了令人瞩目的进展,但特应性疾病的发病机制仍然是一个推测的问题。在一些原发性免疫缺陷病如选择性IgA缺乏症和威斯科特-奥尔德里奇综合征中频繁发现特应性疾病,为研究特应性发生的免疫机制提供了独特的机会。最近对选择性IgA缺乏症患者的研究对特应性是分泌性免疫系统“免疫排斥”缺陷的结果这一广为人知的假说提出了挑战。在与特应性疾病相关的原发性免疫缺陷病中发现的一些免疫学特征表明,调节反应素反应的稳态机制缺陷可能在特应性发病机制中起主要作用。对这些疾病组合进行全面分析可能有助于产生关于特应性疾病免疫发病机制的新的工作假说。