Grünig G, Warnock M, Wakil A E, Venkayya R, Brombacher F, Rennick D M, Sheppard D, Mohrs M, Donaldson D D, Locksley R M, Corry D B
Department of Medicine, San Francisco General Hospital, University of California San Francisco, San Francisco, CA 94143, USA.
Science. 1998 Dec 18;282(5397):2261-3. doi: 10.1126/science.282.5397.2261.
The pathogenesis of asthma reflects, in part, the activity of T cell cytokines. Murine models support participation of interleukin-4 (IL-4) and the IL-4 receptor in asthma. Selective neutralization of IL-13, a cytokine related to IL-4 that also binds to the alpha chain of the IL-4 receptor, ameliorated the asthma phenotype, including airway hyperresponsiveness, eosinophil recruitment, and mucus overproduction. Administration of either IL-13 or IL-4 conferred an asthma-like phenotype to nonimmunized T cell-deficient mice by an IL-4 receptor alpha chain-dependent pathway. This pathway may underlie the genetic associations of asthma with both the human 5q31 locus and the IL-4 receptor.
哮喘的发病机制部分反映了T细胞细胞因子的活性。小鼠模型支持白细胞介素-4（IL-4）和IL-4受体参与哮喘发病。IL-13是一种与IL-4相关且也与IL-4受体α链结合的细胞因子，对其进行选择性中和可改善哮喘表型，包括气道高反应性、嗜酸性粒细胞募集和黏液过度产生。给予IL-13或IL-4均可通过IL-4受体α链依赖性途径使未免疫的T细胞缺陷小鼠呈现哮喘样表型。该途径可能是哮喘与人类5q31基因座和IL-4受体之间遗传关联的基础。
