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Abstract
MicroRNA miR-155 is an important regulatory molecule in the immune system and is highly expressed and functional in Th17 cells, a subset of CD4+ T helper cells which are key players in autoimmune diseases. Small molecules that can modulate miR-155 may potentially provide new therapeutic avenues to inhibit Th17 cell-mediated autoimmune diseases. Here, we present a novel high-throughput screening assay using primary T cells from genetically engineered Mir155 reporter mice, and its use to screen libraries of small molecules to identify novel modulators of Th17 cell function. We have discovered a chemical series of (E)-1-(phenylsulfonyl)-2-styryl-1H-benzo[d] imidazoles as novel down-regulators of Mir155 reporter and cytokine expression in Th17 cells. In addition, we found that FDA approved antiparasitic agents belonging to the ‘azole’ family also down-regulate Mir155 reporter and cytokine expression in Th17 cells, and thus could potentially be repurposed to treat Th17-driven immunopathologies.
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Details
1 National Center for Advancing Translational Sciences (NCATS), NIH, Division of Preclinical Innovation, Rockville, USA (GRID:grid.429651.d) (ISNI:0000 0004 3497 6087)
2 National Institute of Allergy and Infectious Diseases, NIH, Laboratory of Immune System Biology, Bethesda, USA (GRID:grid.419681.3) (ISNI:0000 0001 2164 9667)
3 National Cancer Institute, National Institutes of Health, Experimental Immunology Branch, Bethesda, USA (GRID:grid.48336.3a) (ISNI:0000 0004 1936 8075)