Cytokines in asthma
Cytokines in asthma
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DOI：
10.1183/09031936.01.00229601
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发表时间：
2001-12-01
影响因子：
24.3
通讯作者：
Kips, JC
中科院分区：
文献类型：
--
作者：
Kips, JC
哮喘的气道炎症是由相互作用的细胞因子网络调节的。每种细胞因子在该病发病机制中的确切功能作用尚待完全确定，目前认为2型辅助性T细胞在这一过程中起着至关重要的作用。在giro动物数据表明，白细胞介素（IL）-4和IL-5的诱导过敏原诱导的气道变化的顺序参与。其他2型辅助性T细胞样细胞因子在哮喘中的潜在作用越来越被认识到。特别地，IL-4和IL-13显示出很大程度的冗余。而IL-4似乎是至关重要的主要过敏原致敏过程中，IL-13可能是更重要的二次暴露于雾化过敏原。动物模型也表明，T细胞衍生的细胞因子的生产，而不是嗜酸性粒细胞流入或免疫球蛋白-E的合成，是因果关系改变气道behaviors.An一个重要的方面时，评价细胞因子在一个复杂的疾病，如哮喘的功能作用是与其他细胞因子的微环境中的相互作用。促炎性细胞因子如肿瘤坏死因子-α的表达增加可进一步增强炎症过程，并且与疾病严重程度的联系越来越紧密。此外，免疫调节细胞因子，包括白细胞介素-12，白细胞介素-18或干扰素γ的表达减少也可以加强2型T辅助细胞驱动的炎症过程。
The airway inflammation underlying asthma is regulated by a network of mutually interacting cytokines. The exact functional role of each individual cytokine in the pathogenesis of the disease remains to be fully established.Type 2 T-helper cells are currently considered to play a crucial role in this process. In giro animal data suggest a sequential involvement of interleukin (IL)-4 and IL-5 in the induction of allergen-induced airway changes. The potential role of other type 2 T-helper cell-like cytokines in asthma is increasingly being recognized. In particular, IL-4 and -13 display a large degree of redundancy. Whereas IL-4 seems to be crucial in the primary allergen sensitization process, IL-13 might be more important during secondary exposure to aerosolized allergen. Animal models also indicate that T-cell-derived cytokine production, rather than eosinophil influx or immunoglobulin-E synthesis, is causally related to altered airway behaviour.An important aspect when evaluating the functional role of cytokines in a complex disease such as asthma is the interaction with other cytokines in the microenvironment. Increased expression of pro-inflammatory cytokines such as tumour necrosis factor-alpha can further enhance the inflammatory process, and is increasingly linked to disease severity. In addition, decreased expression of immunoregulatory cytokines, including interleukin-12, interleukin-18 or interferon gamma could also strengthen the type 2 T-helper cell-driven inflammatory process.