The immune system plays a central role in pancreatic diseases. In type 1 diabetes, the immune system attacks the pancreas, destroying insulin-producing beta cells through an autoimmune response. In pancreatic ductal adenocarcinoma, the immune system is silenced, allowing tumours to grow unchecked in one of the most immunosuppressive microenvironments known in cancer biology.

Same organ, mirrored immune failures, we find this duality fascinating. By studying both sides, autoimmune destruction and immune evasion, we look for shared mechanisms, common cellular players, and convergent signalling pathways that might connect what have traditionally been treated as entirely separate diseases.

How does the pancreatic microenvironment shape immune cell behaviour? What determines whether the immune response is destructive, protective, or absent? And can insights from one disease inform therapeutic strategies for the other? These are the questions driving this pillar.

This is where our work becomes inherently collaborative. Immunology, cancer biology, and metabolic disease rarely sit in the same lab.. We actively seek out collaborators who think differently from us, because these questions demand it.