Programming for responsiveness to environmental antigens that trigger allergic respiratory disease in adulthood is initiated during the perinatal period
Programming for responsiveness to environmental antigens that trigger allergic respiratory disease in adulthood is initiated during the perinatal period
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DOI：
10.2307/3434191
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发表时间：
1998-06-01
影响因子：
10.4
通讯作者：
Holt, PG
中科院分区：
文献类型：
--
作者：
Holt, PG
对空气传播的环境抗原（过敏原）过敏是儿童和成人哮喘的主要原因。本综述认为，易发生过敏的过敏原特异性免疫记忆的形成是婴儿期 T 细胞选择过程的最终结果，该过程是通过不成熟的免疫系统与环境中传入的空气传播过敏原之间的相遇而触发的。在正常个体中，这一过程会导致过敏原特异性 T 记忆细胞的发育，从而确保细胞因子的 T 辅助细胞 (Th)-1 模式，从而积极抑制诱导过敏的 Th-2 细胞因子分泌细胞的生长。然而，这些保护性过敏原反应性 Th-1 记忆细胞在某些个体中无法发育，导致过敏原特异性 Th-2 细胞随后增殖，从而引发过敏反应。最近的证据表明，过敏的遗传倾向可能部分是由于子宫内运作的控制机制过度活跃，这些机制通常保护胎儿胎盘单位免受 Th-1 细胞因子的毒性作用。
Allergy to airborne environmental antigens (allergens) is a major cause of asthma in children and adults. This review argues that the development of allergen-specific immunologic memory of the type that predisposes to allergy development is the end result of a T-cell selection process operative during infancy, which is triggered via encounters between the immature immune system and incoming airborne allergens from the environment. In normal individuals this process leads to the development of allergen-specific T-memory cells that secure the T helper (Th)-1 pattern of cytokines, which actively suppress the growth of their allergy-inducing Th-2 cytokine-secreting counterparts. However, these protective allergen-reactive Th-1 memory cells fail to develop in some individuals, permitting the subsequent proliferation of allergen-specific Th-2 cells that can trigger allergic reactions. Recent evidence suggests that genetic predisposition to allergy may be due in part to hyperactivity of control mechanisms operative in utero and which normally protect the fetoplacental unit against the toxic effect of Th-1 cytokines.