Wilson Mark S, Maizels Rick M
Institute of Immunology and Infection Research, University of Edinburgh, Edinburgh, UK.
Chem Immunol Allergy. 2006;90:176-195. doi: 10.1159/000088892.
The inverse relationship between helminth infection and overt allergic reactivity has intrigued medical scientists for three decades. In the past 5 years, detailed epidemiological studies coupled with new experimental model approaches, have substantiated the negative effects of infection on allergic disease manifestation, and begun to provide mechanistic explanations for this fascinating interaction. Several key conclusions can now be drawn. First, the modulation of allergies, such as Th2-dependent pathologies, is not primarily through immune deviation (e.g. switching responsiveness to Th1), as helminth infections themselves drive strong Th2 responses. Second, helminth-infected hosts show similar levels of immune sensitisation to allergens as do uninfected counterparts, but the expression of overt allergic reactivity is suppressed. Third, the down-modulation of allergy in both human and experimental infections is consistent with the activity of T regulatory (Treg) cell populations, which suppress effector mechanisms of both Th1 and Th2 type.
蠕虫感染与明显的过敏反应性之间的反比关系已吸引医学科学家长达三十年之久。在过去五年中,详细的流行病学研究结合新的实验模型方法,证实了感染对过敏性疾病表现的负面影响,并开始为这种迷人的相互作用提供机制解释。现在可以得出几个关键结论。首先,对过敏的调节,如Th2依赖性病理,并非主要通过免疫偏离(例如将反应性转换为Th1),因为蠕虫感染本身会引发强烈的Th2反应。其次,感染蠕虫的宿主对过敏原的免疫致敏水平与未感染的宿主相似,但明显的过敏反应性表达受到抑制。第三,在人类和实验性感染中,过敏的下调与T调节(Treg)细胞群体的活性一致,Treg细胞群体可抑制Th1和Th2型效应机制。