The immune system protects the body from infections and diseases. Helper T cells play an essential role in coordinating immune responses. In adaptive immunity, helper T cells are arguably the most important, as they are required for all adaptive immune responses. T cells activate and produce interleukin-2 (IL-2), a growth factor that causes T cells to proliferate rapidly when the body faces pathogen invasion. T cells trigger pro-inflammatory cytokine release that fights infection. However, constant T cell activation leads to an uncontrolled high amount of pro-inflammatory cytokines, causing tissue damage, resulting in chronic inflammation and, eventually, autoimmune disorders.

We previously found that nebivolol suppressed the pro-inflammatory cytokine, interleukin-17A which is implicated in the pathophysiology of inflammatory diseases and autoimmunity. Currently, there is little known about the effect of nebivolol on T cell activation regarding IL-2 production. In this thesis, I assess whether the immunomodulatory role of nebivolol extends to the IL-2 levels in T cells. My findings demonstrate that nebivolol suppressed IL-2 production in Jurkat T cells, and an inhibitory trend was observed in peripheral blood mononuclear cells (PBMCs) on activated T cells. I also found that nebivolol suppressive activity was β2-adrenergic receptor-dependent, which also implicated nuclear factor kappa B (NFκB) activity, as observed by its inhibition on phosphorylation levels.

These results are novel because there has not been a study on how nebivolol modulates IL-2 levels through the β2-adrenergic receptor. In particular, these findings add to our previous study demonstrating nebivolol immunomodulatory activity on T cells.