Umetsu Dale T, McIntire Jennifer J, Akbari Omid, Macaubas Claudia, DeKruyff Rosemarie H
Division of Immunology and Allergy, Department of Pediatrics, Stanford University, Stanford, CA 94305-5208, USA.
Nat Immunol. 2002 Aug;3(8):715-20. doi: 10.1038/ni0802-715.
The remarkable increase in asthma prevalence that has occurred over the last two decades is thought to be caused by changes in the environment due to improved hygiene and fewer childhood infections. However, the specific infections that limit T helper type 2 (T(H)2)-biased inflammation and asthma are not fully known. Infectious organisms, including commensal bacteria in the gastrointestinal tract and hepatitis A virus, may normally induce the development of regulatory T (T(R)) cells and protective immunity that limit airway inflammation and promote tolerance to respiratory allergens. In the absence of such infections, T(H)2 cells--which are developmentally related to T(R) cells--develop instead and coordinate the development of asthmatic inflammation.
在过去二十年中，哮喘患病率显著上升，人们认为这是由于卫生条件改善和儿童感染减少导致的环境变化所致。然而，具体哪些感染会限制2型辅助性T（Th2）细胞偏向性炎症反应和哮喘，目前尚不完全清楚。包括胃肠道共生菌和甲型肝炎病毒在内的感染性生物体，通常可能诱导调节性T（Treg）细胞的发育和保护性免疫，从而限制气道炎症并促进对呼吸道过敏原的耐受性。在缺乏此类感染的情况下，与Treg细胞在发育上相关的Th2细胞反而会发育，并协调哮喘炎症的发展。
