Airway inflammation in asthma involves complex, interactive, and redundant cascades mediated by an array of proinflammatory cytokines, including a type 2 (T2) pattern of injury. T2 inflammation is characterized by elevations in absolute peripheral or sputum eosinophil counts and levels of IgE (total and allergen-specific) and fractional exhaled nitric oxide, which serve as biomarkers for the presence of this type of inflammation. T2 inflammation is mediated by key “downstream” cytokines, particularly IL-4, IL-5, and IL-13, which act at the effector cell level, as well as upstream cytokines, or “alarmins,” such as thymic stromal lymphopoietin, IL-25, and IL-33 generated by epithelial cells. The relevance of these pathways has led to the development of biologic therapies targeting these T2 cytokines, which have not only resulted in modifying these biomarker signatures for inflammation but have also reduced the disease burden associated with asthma exacerbations, systemic corticosteroid use, and lung function compromises. This review will summarize experiences with anticytokine biologics to highlight which specific asthma outcomes they affect and how these effects reflect inflammatory pathways modified by biologics and may relate to pathophysiologic features of asthma.

哮喘中的气道炎症涉及由一系列促炎细胞因子介导的复杂、相互作用和冗余的级联反应，包括 2 型 (T2) 损伤模式。T2 炎症的特征是绝对外周或痰嗜酸性粒细胞计数和 IgE（总和过敏原特异性）水平和呼出气一氧化氮水平升高，它们可作为此类炎症存在的生物标志物。T2 炎症由关键的“下游”细胞因子介导，特别是 IL-4、IL-5 和 IL-13，它们在效应细胞水平上起作用，以及上游细胞因子或“警报素”，如胸腺基质淋巴细胞生成素，上皮细胞产生的 IL-25 和 IL-33。这些通路的相关性导致了针对这些 T2 细胞因子的生物疗法的发展，这不仅改变了炎症的这些生物标志物特征，而且还减少了与哮喘恶化、全身性皮质类固醇使用和肺功能损害相关的疾病负担。这篇综述将总结抗细胞因子生物制剂的经验，以突出它们影响哪些特定的哮喘结果，以及这些影响如何反映由生物制剂改变的炎症通路，并可能与哮喘的病理生理特征有关。