OxTalks will soon move to the new Halo platform and will become 'Oxford Events.' There will be a need for an OxTalks freeze. This was previously planned for Friday 14th November – a new date will be shared as soon as it is available (full details will be available on the Staff Gateway).
In the meantime, the OxTalks site will remain active and events will continue to be published.
If staff have any questions about the Oxford Events launch, please contact halo@digital.ox.ac.uk
Most immunotherapy efforts aim to mobilize CD8+ T cells against cancer cells. Many tumors lack many neoantigens, and others are selected for partial or complete loss of MHC I, even before immunotherapy intervention. Checkpoint immunotherapy further exacerbates this problem as it preferentially amplifies CD8 cytotoxic effector cell activity, which targets MHC I presented tumor epitopes, imposing strong selection for loss of MHC I or other antigen presentation functions. Our work focuses on mobilizing NK cells and CD4 T cells to attack tumors. Innate immune system agonists and engineered cytokines synergize in eliciting such responses. I will discuss the impact and mechanisms underlying this approach, as examined in mouse cancer models, and its potential for preventing acquired resistance to checkpoint immunotherapy.
