Interferon-λ (IFN-λ) is a central regulator of mucosal immunity; however, its signaling specificity relative to that of type I interferons is poorly defined. IFN-λ can induce antiviral interferon-stimulated genes (ISGs) in epithelia, while the effect of IFN-λ in non-epithelial cells remains unclear. Here we report that neutrophils responded to IFN-λ. We found that in addition to inducing ISG transcription, IFN-λ (but not IFN-β) specifically activated a translation-independent signaling pathway that diminished the production of reactive oxygen species and degranulation in neutrophils. In mice, IFN-λ was elicited by enteric viruses and acted on neutrophils to decrease oxidative stress and intestinal damage. Thus, IFN-λ acted as a unique immunomodulatory agent by modifying transcriptional and non-translational neutrophil responses, which might permit a controlled development of the inflammatory process.

中文翻译：

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IFN-λ通过非翻译调节中性粒细胞功能抑制肠道炎症。

干扰素-λ（IFN-λ）是黏膜免疫的主要调节因子。但是，它相对于I型干扰素的信号传导特异性定义不清。IFN-λ可以在上皮细胞中诱导抗病毒干扰素刺激基因（ISG），而IFN-λ在非上皮细胞中的作用尚不清楚。在这里我们报道嗜中性粒细胞对IFN-λ有反应。我们发现，除了诱导ISG转录外，IFN-λ（而不是IFN-β）还特异性激活了翻译独立的信号传导途径，从而减少了嗜中性粒细胞中活性氧的产生和脱粒。在小鼠中，IFN-λ是由肠病毒引起的，并作用于嗜中性粒细胞以降低氧化应激和肠道损伤。因此，IFN-λ通过修饰转录和非翻译嗜中性粒细胞反应而充当独特的免疫调节剂，