Ngoc P Ly, Gold Diane R, Tzianabos Arthur O, Weiss Scott T, Celedón Juan C
Channing Laboratory, Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115, USA.
Curr Opin Allergy Clin Immunol. 2005 Apr;5(2):161-6. doi: 10.1097/01.all.0000162309.97480.45.
This review examines recent articles on the relationship of cytokines to allergy and asthma with particular emphasis on immune mechanisms involved in disease development in early life.
It was previously proposed that reduced microbial exposure in early life is responsible for a shift of the Th1/Th2 balance in the immune system towards the proallergenic Th2 response. This Th1/Th2 imbalance results in the clinical expression of allergy and/or asthma. In recent years, accumulating data from mice and humans have identified Th2 cytokines [interleukin (IL)-4, IL-13, and IL-5] as major contributors to allergy and asthma. Interestingly, the Th1 cytokine interferon-gamma has recently been shown to act concurrently with Th2 cytokines in maintaining the chronic inflammatory response in allergic diseases, particularly in asthmatic airways. Most recently, evidence suggests that suppression of T-regulatory cells may contribute to the underlying immune mechanisms involved in allergy and asthma.
An enhanced Th2 immune response and the elaboration of cytokines such as IL-4, IL-13, and IL-5 contribute to the induction of allergy and asthma. Interferon-gamma, a Th1 cytokine, acts in conjunction with Th2 (IL-4, IL-13, and IL-5) in maintaining chronic allergic inflammation. The mechanisms leading to an enhanced Th2 response are still controversial. Th2-dominated immune responses may result from immune suppression of T-regulatory cells as well as Th1 cells. Understanding early-life immune mechanisms responsible for atopic diseases, specifically how cytokines of T-regulatory cells act to balance the Th1 and Th2 immune response, continues to be a fruitful area of research.
本综述探讨了近期关于细胞因子与过敏和哮喘关系的文章，特别强调了生命早期疾病发展过程中涉及的免疫机制。
此前有人提出，生命早期微生物接触减少会导致免疫系统中Th1/Th2平衡向促过敏的Th2反应偏移。这种Th1/Th2失衡会导致过敏和/或哮喘的临床表现。近年来，来自小鼠和人类的越来越多的数据表明，Th2细胞因子[白细胞介素（IL）-4、IL-13和IL-5]是过敏和哮喘的主要促成因素。有趣的是，最近研究表明Th1细胞因子干扰素-γ在维持过敏性疾病，特别是哮喘气道的慢性炎症反应中，与Th2细胞因子共同发挥作用。最近，有证据表明T调节细胞的抑制可能与过敏和哮喘的潜在免疫机制有关。
增强的Th2免疫反应以及IL-4、IL-13和IL-5等细胞因子的分泌有助于引发过敏和哮喘。Th1细胞因子干扰素-γ与Th2（IL-4、IL-13和IL-5）共同作用维持慢性过敏性炎症。导致Th2反应增强的机制仍存在争议。以Th2为主的免疫反应可能是由于T调节细胞以及Th1细胞的免疫抑制所致。了解导致特应性疾病的生命早期免疫机制，特别是T调节细胞的细胞因子如何平衡Th1和Th2免疫反应，仍然是一个富有成果的研究领域。
