Coupling dead cell recognition to Fcγ receptors augments anticancer immunity.
- Open access
F-actin-FcγR bridging enhances anticancer immunity by redirecting abundant tumor-associated APCs to cross-present necrotic tumor antigens, improving tumor control in mouse models.
- Why it matters: Limited presence of specialized dendritic cells like cDC1s hampers effective anticancer immune responses. Harnessing other APCs could overcome this barrier and boost immunotherapy outcomes.
- What they did: Researchers used reagents such as Fc-DNGR-1 fusion proteins and anti-F-actin antibodies to connect F-actin on dead cells to Fcγ receptors on various APCs, enabling cross-presentation of tumor antigens in vivo.
- The result: This approach increased tumor control and worked synergistically with chemotherapy or radiotherapy, demonstrating a strategy to amplify anticancer immunity by engaging nonspecialized APCs.