Long, non-coding RNAs (lncRNAs) are involved in the regulation of many cellular processes. The lncRNA IFNG-AS1 was found to strongly influence the responses to several pathogens in mice by increasing interferon gamma (IFNγ) secretion. Studies have looked at IFNG-AS1 in T cells, yet IFNG-AS1 function in natural killer cells (NKs), an important source of IFNγ, remains unknown. Here, we show a previously undescribed sequence of IFNG-AS1 and report that it may be more abundant in cells than previously thought. Using primary human NKs and an NK line with IFNG-AS1 overexpression, we show that IFNG-AS1 is quickly induced upon NK cell activation, and that IFNG-AS1 overexpression leads to increased IFNγ secretion. Taken together, our work expands IFNG-AS1's activity to the innate arm of the type I immune response, helping to explain its notable effect in animal models of disease.

长的非编码RNA（lncRNA）参与许多细胞过程的调控。发现lncRNA IFNG-AS1通过增加干扰素γ（IFNγ）分泌强烈影响小鼠对几种病原体的反应。研究已经研究了T细胞中的IFNG-AS1，但是尚不清楚IFNG-AS1在自然杀伤细胞（NKs）中的功能，NK是IFNγ的重要来源。在这里，我们显示了先前未描述的IFNG-AS1序列，并报告了它在细胞中的含量可能比以前认为的要丰富。使用原代人NK和具有IFNG-AS1过表达的NK品系，我们显示NK细胞活化后迅速诱导IFNG-AS1，而IFNG-AS1的过表达导致IFNγ分泌增加。综上所述，我们的工作将IFNG-AS1的活性扩展到了I型免疫应答的先天臂，