Oxford Events, the new replacement for OxTalks, will launch on 16th March. From now until the launch of Oxford Events, new events cannot be published or edited on OxTalks while all existing records are migrated to the new platform. The existing OxTalks site will remain available to view during this period.
From 16th, Oxford Events will launch on a new website: events.ox.ac.uk, and event submissions will resume. You will need a Halo login to submit events. Full details are available on the Staff Gateway.
Tissue destruction in immune-mediated disease requires more than the presence of antigen-specific lymphocytes. Lessons from type 1 diabetes and celiac disease show that loss of tolerance—marked by autoreactive or dietary antigen–specific Th1 responses—is necessary but not sufficient for pathology. The magnitude of the CD4⁺ T-cell response, and the signals that amplify it, are decisive because they provide the “license” enabling cytotoxic CD8⁺ T cells (CTLs) to kill. Notably, antigen-specific CTLs can persist in tissues without causing injury unless they receive additional cues. These licensing signals differ from those in lymph nodes and include stress-induced non-classical MHC ligands, NK receptor engagement, and cytokines such as IL-15. This framework helps explain why tumor-specific CTLs often fail to clear cancers and suggests that, beyond checkpoint inhibition, therapies must also target the pathways that license CTLs to execute tissue destruction.
