Nebivolol suppressed IL-17A in all of the samples regardless of ADRB2 polymorphisms.
![flowjo 10 百度 flowjo 10 百度](https://exp-picture.cdn.bcebos.com/125ed0ecd3d96975c5deba2fd243040149fe09b0.jpg)
Cellular proliferation and viability was not significantly changed by nebivolol. The ability of nebivolol to inhibit IL-17A was attenuated by a β2AR-specific antagonist. When applied to activated-PBMCs, nebivolol inhibited IL-17A but did not significantly inhibit IFNγ although a trend was observed. Nebivolol inhibited IL-17A and IFNγ from activated Th cells. In contrast, it increased IL-17A in PBMC homozygous for Gly16 codon of ADRB2. Terbutaline consistently inhibited IFNγ from activated PBMC samples. Cytokine response to drug was analyzed based on ADRB2 polymorphisms. Genomic ADRB2 and its immediate upstream region were sequenced using Sanger's method. Cytokines IL-17A and IFNγ were measured using enzyme-linked immunosorbent assay. Terbutaline, a β2AR agonist or nebivolol, a β1AR antagonist and β2AR inverse-agonist, were added in vitro.
![flowjo 10 百度 flowjo 10 百度](https://exp-picture.cdn.bcebos.com/2184380f8835dd8ae00813b103013870d441876c.jpg)
Peripheral blood mononuclear cells (PBMCs) from venous blood of healthy human participants were cultured with T cell activators anti-CD3 and anti-CD28 antibodies. We compared a β2AR agonist to an inverse-agonist, and assessed the influence of ADRB2 polymorphisms on IL-17A and IFNγ responses. Agonists of the β2AR decrease IFNγ but can increase IL-17A from Th cells. Th Cells express the β2-adrenergic receptor (β2AR) that is encoded by ADRB2. Adrenergic drugs are emerging as immunomodulatory agents to treat pro-inflammatory diseases, but their function is not completely understood. Upon activation, helper T (Th) cells produce cytokines such as IL-17A and IFNγ, which may exacerbate inflammatory disease and disorders.