On 28th November OxTalks will move to the new Halo platform and will become 'Oxford Events' (full details are available on the Staff Gateway).
There will be an OxTalks freeze beginning on Friday 14th November. This means you will need to publish any of your known events to OxTalks by then as there will be no facility to publish or edit events in that fortnight. During the freeze, all events will be migrated to the new Oxford Events site. It will still be possible to view events on OxTalks during this time.
If you have any questions, 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.
