Regulatory T cells (Tregs) expressing the transcription factor Foxp3 are indispensable for the prevention of auto-immunity, as exemplified by the uncontrolled immune activation and severe pathologies in Treg-impaired individuals bearing FOXP3 mutations. Importantly, the immunosuppressive capacity of Tregs extends beyond controlling autoimmune diseases, and includes curtailing inflammation after infection, as well as inhibiting CD8⁺ T cell-driven anti-tumour immunity, amongst others. Emerging studies have revealed the presence of tissue-resident regulatory T cells (trTregs), a distinct Treg subset that populates non-lymphoid tissues. In addition to immune-suppression, trTregs are critical regulators of organ homeostasis and tissue-repair. Yet many questions persist about how trTreg locally engage with immune and parenchymal cells to resolve different types of inflammation. On one hand, we found that during lung allergic inflammation, trTreg engage with type-2 innate lymphoid cells (ILC2s) via the OX40-OX40L pathway to restrain adaptive type-2 immunity. On the other hand, we identified a previously unappreciated crosstalk between pancreatic trTregs and acinar cells, which is mandatory for tissue repair in contexts of acute pancreatitis and pancreatic cancer. In all, our work reveals novel insights into the function and regulation of trTregs, which is of particular translational relevance given the ever-increasing interest into therapies aiming at modulating Treg numbers or function.

The seminar will be held at the Amphi of the ICAB (not Léon Fredericq)