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Elucidating a role for a hematopoietic-tropic microRNA in T cell (IRM12P.650)

To gain new insight into how miRNA impact T cell responses, mice were immunized with costimulation and adjuvant to generate potent T effector responses. We generated a cDNA library from lymphoid tissue. Using sequencing of size-fractionated cDNA we cloned 6 potential new miRNAs with characteristic stem loop folding. One of these candidates, termed miR-R89 but not yet registered in miRBase, was unique since its expression was hematopoietic specific and regulated during immune activation. The targets and function of miR-R89 are currently unknown, but our preliminary data show it is expressed in a T cell clone known to cause experimental autoimmune encephalitis. Transfection with a locked nucleic acid (LNA) mimic of miR-R89 in EL4 thymoma cells increased IL-2 secretion after PMA-ionomycin (PI) stimulation compared to transfection with control LNA. RNAseq analysis of the transfected cells revealed that mRNA expression of two transcription factors involved in metabolism, Tfe3 and Tef, was reduced by miR-R89 mimic. Interestingly, 3’UTR mRNA of Tfe3 and Tef have several theoretical binding sites for miR-R89. Treatment of PI-stimulated EL4 cells with UK5099, an inhibitor of mitochondrial pyruvate transport and metabolism, mediated a similar increase of IL-2 secretion than observed after transfection with miR-R89. These data suggest the putative miRNA miR-R89 could target Tfe3 and Tef mRNA and function as a metabolic regulator of T cell activation.