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IFNG-AS1 Enhances Interferon Gamma Production in Human Natural Killer Cells. 2019

Natan Stein, and Orit Berhani, and Dominik Schmiedel, and Alexandra Duev-Cohen, and Einat Seidel, and Inbal Kol, and Pinchas Tsukerman, and Merav Hecht, and Adi Reches, and Moriya Gamliel, and Akram Obeidat, and Yoav Charpak-Amikam, and Rachel Yamin, and Ofer Mandelboim
The Lautenberg Center for General and Tumor Immunology, Institute for Medical Research Israel-Canada, The Hebrew University Hadassah Medical School, Jerusalem 9112001, Israel.

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.

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