Chromatin accessibility analysis of MIAT sufficient and MIAT deficient Th17 cells by ATAC-seq

T helper 17 (Th17) cells protect against fungal and bacterial infections and are implicated in autoimmunity. Several long intergenic noncoding RNAs (lincRNA) are induced during Th17 differentiation, however, their contribution to Th17 differentiation is poorly understood. We discovered a lincRNA myocardial infarction associated transcript (MIAT) to be upregulated early after induction of human Th17 cell differentiation along with an increase in the chromatin accessibility at the gene locus. We found that MIAT deficiency leads to chromatin accessibility at several loci including IL17A promoter. Overall design: CD4 T cells were isolated using magnetic bead-based positive selection kit from Dynal. Cells were nucleofected with the two antisense locked nuelceic acid (LNAs) targeting the lincRNA MIAT or non targeting control LNAs (NC). After 48 hours of rest, cells were differentiated to Th17 for 24 hours or 72 hours. There were three biological replicates. Three LNAs * two time points* three replicates =18 samples.