Wills-Karp M, Luyimbazi J, Xu X, Schofield B, Neben T Y, Karp C L, Donaldson D D
Department of Environmental Health Sciences, Johns Hopkins University School of Hygiene and Public Health, Baltimore, MD 21205, USA.
Science. 1998 Dec 18;282(5397):2258-61. doi: 10.1126/science.282.5397.2258.
The worldwide incidence, morbidity, and mortality of allergic asthma are increasing. The pathophysiological features of allergic asthma are thought to result from the aberrant expansion of CD4(+) T cells producing the type 2 cytokines interleukin-4 (IL-4) and IL-5, although a necessary role for these cytokines in allergic asthma has not been demonstrable. The type 2 cytokine IL-13, which shares a receptor component and signaling pathways with IL-4, was found to be necessary and sufficient for the expression of allergic asthma. IL-13 induces the pathophysiological features of asthma in a manner that is independent of immunoglobulin E and eosinophils. Thus, IL-13 is critical to allergen-induced asthma but operates through mechanisms other than those that are classically implicated in allergic responses.
过敏性哮喘的全球发病率、发病率和死亡率正在上升。过敏性哮喘的病理生理特征被认为是由产生2型细胞因子白细胞介素-4（IL-4）和IL-5的CD4(+) T细胞异常扩增所致，尽管这些细胞因子在过敏性哮喘中的必要作用尚未得到证实。2型细胞因子IL-13与IL-4共享受体成分和信号通路，被发现对过敏性哮喘的表达是必要且充分的。IL-13以一种独立于免疫球蛋白E和嗜酸性粒细胞的方式诱导哮喘的病理生理特征。因此，IL-13对变应原诱导的哮喘至关重要，但通过不同于经典过敏反应所涉及的机制发挥作用。
