This study examined the role of CCR7+ activated dendritic cells (actDCs) — a convergent activation state shared by cDC1s and cDC2s — in anti-tumor immunity, using mouse models that conditionally labeled or ablated actDCs via CCR7 expression.
Only actDCs (not resting cDCs) could stimulate tumor-specific cytotoxic T lymphocytes (CTLs); cDC1-derived actDCs used cross-presentation while cDC2-derived actDCs used cross-dressing (cancer type-dependent). Ablation of actDCs impaired spontaneous tumor control and blunted responses to immune checkpoint blockade and adoptive T cell therapy.
Findings are from mouse models; direct translation to human tumor immunology requires validation. The cancer type-dependence of cDC2-mediated cross-dressing is not fully characterized. Conditional ablation via CCR7 may affect non-DC CCR7+ cells.
actDC abundance or function may serve as a biomarker for checkpoint blockade or adoptive T cell therapy response. Strategies to expand or preserve the actDC state in tumors could enhance immunotherapy efficacy.
