The dimeric cytokine interleukin (IL)-26 belongs to the IL-10 family. Whereas it was originally perceived as a T-helper (Th)17 cytokine, subsequent studies have shown that IL-26 is produced by several populations of leukocytes and structural cells. This cytokine binds to a heterodimeric receptor complex including IL-10R2 and -20R1 (IL-26R) and signals through STAT 1 and 3 to induce the release of chemokines and growth factors. Remarkably, IL-26 directly kills bacteria and inhibits viral replication. The most recent studies on human airways confirm multiple cellular sources in this critical interphase of host defense and demonstrate that stimulation of toll-like receptors (TLR) trigger the release of IL-26. Once released, it exerts a dualistic effect on cytokine production and up-regulates gene expression of IL-26R. It also potentiates chemotaxis and inhibits chemokinesis for neutrophils, thereby facilitating the accumulation of innate effector cells at the site of bacterial stimulation. The high levels of IL-26 in human airways are altered in inflammatory airway disorders such as asthma and chronic obstructive pulmonary disease. Thus, IL-26 emerges as an important mediator, providing direct and indirect actions on microbes, actions that are essential for host defense and inflammation and bears potential as a biomarker of disease.

二聚体细胞因子白细胞介素 (IL)-26 属于 IL-10 家族。虽然它最初被认为是一种 T 辅助 (Th)17 细胞因子，但随后的研究表明，IL-26 是由几个白细胞和结构细胞群体产生的。这种细胞因子与异二聚体受体复合物结合，包括 IL-10R2 和 -20R1 (IL-26R)，并通过 STAT 1 和 3 发出信号以诱导趋化因子和生长因子的释放。值得注意的是，IL-26 直接杀死细菌并抑制病毒复制。最近对人类呼吸道的研究证实了宿主防御的这个关键相间的多个细胞来源，并证明刺激 Toll 样受体 (TLR) 会触发 IL-26 的释放。一旦释放，它就会对细胞因子的产生产生双重作用，并上调 IL-26R 的基因表达。它还可以增强趋化性并抑制嗜中性粒细胞的趋化作用，从而促进先天效应细胞在细菌刺激部位的积累。人气道中高水平的 IL-26 在炎症性气道疾病（如哮喘和慢性阻塞性肺病）中发生改变。因此，IL-26 成为一种重要的介质，对微生物提供直接和间接作用，这些作用对宿主防御和炎症至关重要，并具有作为疾病生物标志物的潜力。