Adrb1, also known as the β1-adrenergic receptor, is a crucial component in the adrenergic signaling pathway. It binds to catecholamines such as epinephrine and norepinephrine, playing a significant role in regulating various physiological processes including heart rate, cardiac contractility, and the body's stress response. It is also involved in immune-related functions, linking the stress-associated catecholamines to the progression of T-cell exhaustion [1].

In a study on T-cell exhaustion, it was found that exhausted CD8+ T-cells increase ADRB1 expression. Exposure of ADRB1+ T-cells to catecholamines suppresses their cytokine production and proliferation. Ablation of β1-adrenergic signalling limits the progression of T-cells towards the exhausted state in chronic infection and improves effector functions when combined with immune checkpoint blockade in melanoma [1].

In conclusion, Adrb1 is essential for multiple physiological and immune-related functions. Its role in regulating T-cell exhaustion, as revealed through functional studies, has significant implications for understanding and potentially treating diseases related to immune dysfunction such as cancer and chronic infections [1].

References:

1. Globig, Anna-Maria, Zhao, Steven, Roginsky, Jessica, Emu, Brinda, Kaech, Susan M. 2023. The β1-adrenergic receptor links sympathetic nerves to T cell exhaustion. In Nature, 622, 383-392. doi:10.1038/s41586-023-06568-6. https://pubmed.ncbi.nlm.nih.gov/37731001/