ECResearch

In cancer and ageing, tissues become metabolically distorted and enriched in stressed (senescent) cells that release bioactive lipids and inflammatory signals into their environment. These lipids accumulate in age-related pathologies and genetic disorders (e.g. X-linked adrenoleukodystrophy, Zellweger syndrome) that are characterised by premature tissue degeneration, chronic inflammation, fibrosis, and stem cell dysfunction—indicating that these lipids act as causal metabolic stressors.

​

Our research focuses on how lipid metabolic perturbations reprogram T cells, particularly regulatory T cells, and reshape their function with profound consequences for immune surveillance in ageing and cancer. We use advanced microscopy to dissect how lipid-rich, senescent tissues instruct immune cell behaviour at the molecular and cellular level.

​

Our imaging reveals that lipid-driven immune reprogramming is accompanied by striking structural remodelling and reorganisation of:

• The 3D endocytic network (the intracellular transport system) – Fig. 1
• Mitochondria (the cellular energy factories) – Fig. 2
• The nanoscale organisation of T cell receptors (the “on-button” of T cells) – Fig. 3
• Plasma membrane lipid and protein composition and 3D architecture at the immune synapse – Fig. 4

​

By integrating immunometabolism, lipidomics, and immune cell engineering with high-resolution imaging and tissue-mimetic platforms, we aim to define how metabolic signals from senescent tissues drive immune plasticity. Our long-term goal is to uncover general principles of immune–tissue communication and exploit them to restore immune surveillance and tissue homeostasis in cancer and age-associated disease.