Immunotherapy is revolutionizing treatment practice for cancer and a rapidly growing armamentarium of immune-modulating agents are being developed. It is appreciated that tumour-evoked inflammation and immune suppression are major impediments to successful treatment outcomes. The role of neural signalling in these interactions have largely been overlooked, despite the known intricacies of bi-directional regulation between the immune and nervous systems. Our objective for this study was to use an interdisciplinary approach to investigate a causal link between tumour-induced inflammation and neurohormone-mediated immunosuppression in B cell non-Hodgkin’s lymphoma. Focussing on the beta-adrenergic receptor (βAR) pathway of the sympathetic nervous system we have demonstrated that increased βAR signalling in the tumour environment leads to faster outgrowth and dissemination of mouse Eµ-myc lymphoma. The effectiveness of immune checkpoint-modulating immunotherapy against these tumours is also diminished in the presence of chronic peripheral βAR signalling, and this is associated with βAR-mediated suppression of CD8 T cell function. We are currently investigating tumour-evoked inflammatory signals which lead to increased systemic production of neurohormones, as well as the potential for re-purposing beta-blocker drugs for cancer treatment to boost the efficacy of immunotherapy.