Araujo Maria Ilma, de Carvalho Edgar M
Serviço de Imunologia, Hospital Universitário Prof. Edgard Santos, Universidade Federal da Bahia, and Escola Bahiana de Medicina e Saúde Pública, Salvador, BA, Brazil.
Chem Immunol Allergy. 2006;90:29-44. doi: 10.1159/000088879.
Studies have demonstrated that people living in areas endemic for helminths have a decreased reactivity to skin prick tests to aeroallergens and milder forms of asthma. Hypotheses to explain the inverse correlation between helminth infections and atopy include competition between helminth-induced polyclonal IgE and aeroallergen-specific IgE for high-affinity receptors present on mast cells, increased number of regulatory T cells, and high levels of regulatory cytokines, such as IL-10, produced during helminthic infections. Indeed, cells from asthmatic individuals infected with Schistosoma mansoni produce lower levels of IL-5 than asthmatics free of infections. In contrast, IL-10 is more readily produced by allergen-stimulated cells from asthmatics who are infected and is detected only at low levels by cells from helminth-free asthmatics. It is well known that Th2 cytokines are involved in the pathogenesis of allergies and asthma, and some studies indicate that IL-10 is the key cytokine that inhibits the Th2-inflammatory response in allergy. In this chapter we will discuss the association between S. mansoni infection, atopy and severity of asthma and possible mechanisms by which individuals living in helminth endemic areas are protected against the development of allergies.
研究表明，生活在蠕虫流行地区的人对气传变应原的皮肤点刺试验反应性降低，哮喘症状也较轻。解释蠕虫感染与特应性之间负相关的假说包括：蠕虫诱导的多克隆IgE与气传变应原特异性IgE竞争肥大细胞上的高亲和力受体、调节性T细胞数量增加以及蠕虫感染期间产生的高水平调节性细胞因子（如IL-10）。事实上，感染曼氏血吸虫的哮喘患者的细胞产生的IL-5水平低于未感染的哮喘患者。相反，感染的哮喘患者的变应原刺激细胞更容易产生IL-10，而未感染蠕虫的哮喘患者的细胞仅能检测到低水平的IL-10。众所周知，Th2细胞因子参与过敏和哮喘的发病机制，一些研究表明IL-10是抑制过敏中Th2炎症反应的关键细胞因子。在本章中，我们将讨论曼氏血吸虫感染、特应性与哮喘严重程度之间的关联，以及生活在蠕虫流行地区的个体免受过敏发展影响的可能机制。
