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Open AccessArticle

Regulation of KIR3DL3 Expression via miRNA

1
Biomedical Sciences Program, Graduates School of Khon Kaen University, Khon Kaen 40002, Thailand
2
Department of Clinical Immunology and Transfusion Sciences, School of Medical Technology, Faculty of Associated Medical Sciences, Khon Kaen University, Khon Kaen 40002, Thailand
3
The Centre for Research and Development of Medical Diagnostic Laboratories (CMDL), Faculty of Associated Medical Sciences, Khon Kaen University, Khon Kaen 40002, Thailand
4
School of Human Sciences, University of Western Australia, Perth, WA 6009, Australia
5
Institute for Immunology and Infectious Diseases, Murdoch University, Perth, WA 6150, Australia
6
Division of Infectious Diseases, Vanderbilt University Medical Center, Nashville, TN 37232, USA
*
Author to whom correspondence should be addressed.
Genes 2019, 10(8), 603; https://doi.org/10.3390/genes10080603
Received: 16 July 2019 / Revised: 31 July 2019 / Accepted: 5 August 2019 / Published: 9 August 2019
(This article belongs to the Section Molecular Genetics and Genomics)
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Abstract

Killer-cell immunoglobulin-like receptor (KIR) 3DL3 is a framework gene present in all human KIR haplotypes. Although the structure of KIR3DL3 is suggestive of an inhibitory receptor, the function of KIR3DL3 has not been demonstrated and cognate ligands have not been identified. KIR3DL3 has been shown to be constitutively expressed at a low RNA level in peripheral blood mononuclear cell (PBMC) and decidual natural kill (NK) cells, but cell surface expression of KIR3DL3 cannot be detected. Accordingly, post-transcriptional regulation of KIR3DL3 should exist. Using bioinformatics analysis, we identified three candidate micro ribonucleic acids (miRNAs; miR-26a-5p, -26b-5p and -185-5p) that potentially regulate KIR3DL3 expression. Luciferase reporter assays utilizing constructs with mutated miRNA-binding sites of miR-26a-5p, -26b-5p and -185-5p in the 3’-untranslated region (3’ UTR) of KIR3DL3 resulted in up-regulation of luciferase activity demonstrating a potential mechanism of gene regulation. Furthermore, knockdown of the same endogenous miRNAs using silencing ribonucleic acid (siRNA) led to induced surface expression of KIR3DL3. In conclusion, we provide a novel mechanism of functional regulation of KIR3DL3 via miRNAs. These findings are relevant in understanding the generation of KIR repertoire and NK cell clonality. View Full-Text
Keywords: killer-cell immunoglobulin-like receptor (KIR) 3DL3; miRNA; 3’untranslated region; post-transcriptional regulation killer-cell immunoglobulin-like receptor (KIR) 3DL3; miRNA; 3’untranslated region; post-transcriptional regulation
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Nutalai, R.; Gaudieri, S.; Jumnainsong, A.; Leelayuwat, C. Regulation of KIR3DL3 Expression via miRNA. Genes 2019, 10, 603.

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