Bellanti Joseph A, Malka-Rais Jonathan, Castro Henry J, de Inocencio Julia Mendez, Sabra Aderbal
Department of Pediatrics and the International Center for Interdisciplinary Studies of Immunology, Georgetown University Medical Center, Washington, DC 20057, USA.
Ann Allergy Asthma Immunol. 2003 Jun;90(6 Suppl 3):2-6. doi: 10.1016/s1081-1206(10)61652-3.
An increase in prevalence of allergic diseases has been seen at an unprecedented rate in many countries throughout the world. Associated with this increase in allergic disease has been a disturbing increase in morbidity and mortality of such diseases as asthma despite the availability of several new therapeutic agents over the past 2 to 3 decades. The search for both environmental factors, eg, new allergens, as well as biologic markers of genetic susceptibility, eg, respiratory viruses, has yielded considerable promise for an explanation for this rising prevalence of allergic disease.
To present a central unifying hypothesis based upon recent knowledge concerning the developing human immune system and its interaction with external environmental factors, particularly viral infections, as a basis for a clearer understanding of the changing faces of the allergic diseases throughout the lifespan of the individual.
English language articles were selected from PubMed, as well as selected abstracts that would have immediate, practical clinical implications.
Review of the current literature strongly suggests a relationship between delayed acquisition of Th1 function in the allergy-prone infant, not only as a predictive marker of susceptibility to the development of allergic disease but also as an explanation for the unique vulnerability of these infants to viral infection, eg, bronchiolitis. Furthermore, viral infection during early development in the allergy-prone infant appears to facilitate allergic sensitization in early infancy. This interesting triad of immune deficiency, viral infection, and atopic genetic susceptibility may provide a basis for early detection of allergic disease and may offer new intervention strategies for the prevention of allergic and infectious disease in the young infant.
在世界许多国家,过敏性疾病的患病率正以前所未有的速度上升。尽管在过去20至30年中有几种新的治疗药物,但与此相关的是,诸如哮喘等此类疾病的发病率和死亡率却令人不安地增加。对环境因素(如新的过敏原)以及遗传易感性生物标志物(如呼吸道病毒)的研究,为解释过敏性疾病患病率上升提供了很大希望。
基于有关发育中的人类免疫系统及其与外部环境因素(特别是病毒感染)相互作用的最新知识,提出一个核心统一假说,作为更清晰地理解个体一生中过敏性疾病不断变化的基础。
从PubMed中选取英文文章,以及具有直接实际临床意义的精选摘要。
对当前文献的回顾强烈表明,易过敏婴儿Th1功能延迟获得之间存在关联,这不仅是过敏性疾病易感性的预测指标,也是这些婴儿易受病毒感染(如细支气管炎)影响的原因。此外,易过敏婴儿早期发育期间的病毒感染似乎会促进婴儿早期的过敏致敏。这种有趣的免疫缺陷、病毒感染和特应性遗传易感性三联征可能为早期发现过敏性疾病提供基础,并可能为预防幼儿过敏性和感染性疾病提供新的干预策略。