Abstract
Abstract Natural Killer T (NKT) cells are innate-like lymphocytes that rapidly produce cytokines upon activation. However, following primary stimulation with the potent ligand α-galactosylceramide (αGC), NKT cells become hyporesponsive, defined as a severe reduction in effector cytokines upon re-stimulation. The purpose of this project is to investigate the role of microRNAs (miRNAs) during NKT cell transition from effector response, expansion and hyporesponsiveness. MiRNAs are ~22bp non-coding RNAs that associate with the RNA-induced silencing complex (RISC) to inhibit the translation of target transcripts. We performed a Nanostring microRNA analysis to determine global expression of microRNAs in NKT cells after α-GC stimulation. MicroRNA-21 (miR-21) was found to be highly upregulated in splenic NKT cells at 3-hours, 3-day, and 30-days post-activation compared to unstimulated controls. Our preliminary data show that MiR-21KO/KO splenic and liver NKT cells have a lower frequency at day-3 compared to WT-littermate controls. We hypothesize that miR-21 regulates the NKT cell transition from activation to hyporesponsiveness and that miR-21KO/KO NKT cells exhibit an interrupted hyporesponsive state.
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