Advisor - Dr. Jennifer Powell
Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system caused by an autoimmune attack on myelin-producing oligodendrocytes. Most of our understanding of the pathogenesis of multiple sclerosis comes from investigations using the experimental autoimmune encephalomyelitis (EAE) animal model. In this model, both CD4+ T helper type 1 (TH1) and T helper type 17 (TH17) cells contribute to the pathogenesis of the disease. TH1 cells are under the control of the transcription factor T-bet, which also acts to inhibit the TH17 cell lineage. Despite this role as a negative regulator of TH17 differentiation in naïve CD4+ T cells, T-bet regulation plays a critical role in the function of mature TH17 cells. T-bet is re-expressed in TH17 cells in response to IL-23, driving the pathogenesis of autoimmune diseases, including EAE. We looked to the role of microRNAs in the regulation of T-bet expression, specifically microRNA-330, which was identified through a microRNA micro-array. Here, we investigated the role of miR-330 in the regulation of T-bet expression in TH1 and TH17 cells and found a positive correlation between miR-330 and T-bet expression, indicating that miR-330 has an interesting regulatory role in this context.