IGF-1 promotes the development and cytotoxic activity of human NK cells

Fang Ni, Rui Sun, Binqing Fu, Fuyan Wang, Chuang Guo, Zhigang Tian () and Haiming Wei ()
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Fang Ni: Institute of Immunology, School of Life Sciences, University of Science and Technology of China
Rui Sun: Institute of Immunology, School of Life Sciences, University of Science and Technology of China
Binqing Fu: Institute of Immunology, School of Life Sciences, University of Science and Technology of China
Fuyan Wang: Institute of Immunology, School of Life Sciences, University of Science and Technology of China
Chuang Guo: Institute of Immunology, School of Life Sciences, University of Science and Technology of China
Zhigang Tian: Institute of Immunology, School of Life Sciences, University of Science and Technology of China
Haiming Wei: Institute of Immunology, School of Life Sciences, University of Science and Technology of China

Nature Communications, 2013, vol. 4, issue 1, 1-11

Abstract: Abstract Insulin-like growth factor 1 (IGF-1) is a critical regulator of many physiological functions, ranging from longevity to immunity. However, little is known about the role of IGF-1 in natural killer cell development and function. Here, we identify an essential role for IGF-1 in the positive regulation of human natural killer cell development and cytotoxicity. Specifically, we show that human natural killer cells have the ability to produce IGF-1 and that differential endogenous IGF-1 expression leads to disparate cytotoxicity in human primary natural killer cells. Moreover, miR-483-3p is identified as a critical regulator of IGF-1 expression in natural killer cells. Overexpression of miR-483-3p has an effect similar to IGF-1 blockade and decreased natural killer cell cytotoxicity, whereas inhibition of miR-483-3p has the opposite effect, which is reversible with IGF-1 neutralizing antibody. These findings indicate that IGF-1 and miR-483-3p belong to a new class of natural killer cell functional modulators and strengthen the prominent role of IGF-1 in innate immunity.

Date: 2013
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DOI: 10.1038/ncomms2484

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