Abstract

We have previously found that nebivolol inhibits the cytokines of T helper 1 and T helper 17 cells which are linked to autoimmunity and in turn supports nebivolol’s candidacy as a therapeutic of autoimmune diseases such as multiple sclerosis. In this thesis, I aimed to confirm the inhibitory role of nebivolol on T helper cells and explore whether these effects are mediated by nitric oxide induction. The findings of this thesis show that nebivolol inhibited the cytokine production of T helper 17 and T helper 1 cells in samples of human peripheral mononuclear cells. I also found that these effects were not mediated by nitric oxide and its predominant signaling pathway. Instead, a low level of nitric oxide was produced during adrenergic signaling and helped to stabilize T helper 17 and T helper 1 cells. Finally, nebivolol, which has not been investigated before on human immune cells, represents a promising immunomodulatory adrenergic drug that can help to mitigate the symptoms of autoimmune diseases without inducing cell death or altering nitric oxide levels.