Gene expression profiles of Control and FAK KO Th17 cells
T helper type 17 (Th17) cells play critical roles in the pathogenesis of various autoimmune and inflammatory diseases; however, signaling pathways that affect Th17 cell differentiation are not fully understood. Here, we investigated whether focal adhesion kinase (FAK), an integrator of extracellular signals, regulates differentiation of Th17 cells. We measured alteration of gene expression in FAK-deficient Th17 cells compared to WT Th17 cells using RNA-sequencing. Overall design: We isolated naïve CD4 T cells from Fakfl/fl mice and introduced a Cre recombinase-expressing vector into the cells to induce gene deletion (these cells are referred to Fak KO). These cells were stimulated with plate-bound anti-CD3e (10 µg/ml) and soluble anti-CD28 (5 µg/ml) antibodies and cultured for 3 days under Th17-polarizing conditions. Then we harvested the cells and conducted RNA-sequencing (RNA-seq) to identify altered genes in Fak KO Th17 cells.