Jie Yang

Jie Yang originally trained in Veterinary Medicine before undertaking a PhD in Immunology at the Roslin Institute in the University of Edinburgh. Following postdoctoral work at the Francis Crick Institute and the University of Cambridge, he joined the Department of Oncology at the University of Oxford as a Group Leader in 2025.

A major contribution of his research was discovery of the mechanisms underlying the anti-metastatic effects of aspirin. He showed that inhibitors of cyclooxygenase 1 (COX-1), including aspirin, enhance immunity to cancer metastasis by releasing T cells from suppression by platelet-derived thromboxane A2 (Yang et al., Nature 2025). His work contributed to understanding of clinical observations of aspirin’s anti-metastatic effects first reported over 50 years ago and received widespread media attention including BBC News. This work is particularly timely as it provides mechanistic insight for new randomised controlled trials including CaPP3 and Add-Aspirin, which are investigating the efficacy of low-dose aspirin in cancer prevention and recurrence.

In addition, his earlier work revealed molecular mechanisms required for quiescence and long-term survival of Treg cells that drive tumour immunosuppression (Grant and Yang, et al., J Exp Med 2020) and established the critical role of IL-7 signalling in maintaining ILC3 populations required for normal lymphocyte trafficking (Yang et al., J Exp Med 2018). Jie's research has made fundamental contributions to our understanding of immune regulation and cancer immunosuppression.

T cells drive immune responses against cancer, but their function is constrained by immunosuppressive mechanisms that enable cancer progression and metastasis. Our research aims to uncover the molecular and cellular mechanisms underpinning immune regulation and cancer immunosuppression, with the goal of developing new approaches for cancer prevention and treatment of metastatic disease.

Our research vision focuses on:

• Immune-metastasis interactions: Understanding how metastatic cancer cells evade immune surveillance and manipulate local immune environments, and identifying targetable pathways to enhance anti-metastatic immunity.
• Immune-based cancer prevention: Investigating how immune-modulating interventions, including biological therapies and readily available small molecule drugs like aspirin, could prevent cancer development and spread in high-risk populations.
• T cell dysfunction and immune regulation: Identifying novel cellular and molecular inhibitory pathways that constrain cancer immunity and developing translatable therapeutic strategies to improve the efficacy of immunotherapy.