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
The membrane attack complex (MAC) is a large macromolecular immune pore that punches holes in target cells. While a potent weapon of the innate immune defense, MAC pores can also damage human cells if not properly controlled. Here we use cryoEM to understand the molecular basis for how MAC pore formation is controlled in human cells during an immune response. By solving the structure of a soluble regulated form of MAC called sMAC, we explain how blood-based chaperones scavenge and clear potentially harmful complement activation by-products. Most recently we have created a membrane model system with a synthetic GPI-anchored cellular receptor (CD59) that inhibits MAC. Using cryoEM, we
show how CD59 captures and deflects pore-forming beta-hairpins of complement proteins, rerouting their membrane trajectory. Moreover, we have discovered how the membrane environment influences the role of CD59 in complement regulation and in host-pathogen interactions. Our results open new lines of investigation into the importance of lipids in immune homeostasis that may be relevant for therapies that
regulate complement.
