Coupling dead cell recognition to Fcγ receptors augments anticancer immunity.

F-actin-FcγR bridging enhances tumor control and synergizes with therapy in mouse cancer models.

• Why it matters: Limited presence of cDC1s in tumors restricts anticancer immunity, prompting the need to harness other APCs for cross-presentation of tumor antigens.
• What they did: Researchers used reagents, including Fc-DNGR-1 fusion protein and anti-F-actin antibody, to redirect abundant tumor-associated APCs such as cDC2s and monocyte-derived cells to internalize necrotic debris and cross-present antigens in vivo.
• The result: F-actin-FcγR bridging improves tumor control and works synergistically with chemotherapy or radiotherapy, suggesting a strategy to boost anticancer immunity by engaging nonspecialized APCs.