Wills-Karp Marsha
Division of Immunobiology, Children's Hospital Medical Center, 3333 Burnett Avenue, MLC 7038, Cincinnati, OH 45208, USA.
Curr Allergy Asthma Rep. 2004 Mar;4(2):123-31. doi: 10.1007/s11882-004-0057-6.
Numerous studies have clearly shown that the Th2 cytokine, interleukin (IL)-13, is the central regulator of the allergic diathesis. Initial studies in animal models of disease provided compelling evidence that IL-13, independent of other Th2 cytokines, was both necessary and sufficient to induce all features of allergic asthma. The importance of IL-13 in allergic disorders in humans is supported by consistent associations between tissue IL-13 levels and genetic variants in the IL-13 gene with asthma and related traits. With the preponderance of evidence continuing to support the importance of IL-13 in allergic disorders, attention is now turned toward understanding the mechanisms by which this cytokine might mediate the pathophysiologic features of allergic disease. The emerging paradigm is that IL-13 induces features of the allergic response via its actions on epithelial cells and smooth muscle cells, not through traditional effector pathways involving eosinophils and IgE-mediated events. In light of these recent developments, in this review our current understanding of the role of IL-13 in the pathogenesis of asthma is explored, with a particular focus on new insights into the mechanisms by which IL-13 induces the features of asthma.
大量研究已明确表明，Th2细胞因子白细胞介素（IL）-13是过敏性素质的核心调节因子。对疾病动物模型的初步研究提供了令人信服的证据，即IL-13独立于其他Th2细胞因子，对于诱导过敏性哮喘的所有特征既必要又充分。组织IL-13水平以及IL-13基因中的遗传变异与哮喘及相关特征之间的持续关联，支持了IL-13在人类过敏性疾病中的重要性。由于大量证据继续支持IL-13在过敏性疾病中的重要性，现在人们的注意力转向了解这种细胞因子可能介导过敏性疾病病理生理特征的机制。新出现的模式是，IL-13通过其对上皮细胞和平滑肌细胞的作用来诱导过敏反应特征，而不是通过涉及嗜酸性粒细胞和IgE介导事件的传统效应途径。鉴于这些最新进展，在本综述中，我们探讨了目前对IL-13在哮喘发病机制中作用的理解，特别关注对IL-13诱导哮喘特征机制的新见解。
