Immune checkpoint inhibitors are successful immunotherapy modalities that enhance CD8þ T-cell responses. Although T cells are initially primed in draining lymph nodes, the mechanisms that underlie their reactivation inside the tumor microenvironment are less clear. Recent studies have found that not only is the cross-priming of conventional type 1 dendritic cells (cDC1) required to initiate CD8þ T-cell responses during tumor progression, but it also plays a central role in immunotherapy-mediated reactivation of tumor-specific CD8þ T cells for tumor regression. Moreover, many cancer treatment modalities trigger type I IFN responses, which play critical roles in boosting cDC1 cross-priming and CD8þ T-cell reactivation. Inducing type I IFNs within tumors can overcome innate immune resistance and activate antitumor adaptive immunity. Here, we review recent studies on how type I IFN-cDC1 cross-priming reactivates CD8þ T cells and contributes to tumor control by cancer immunotherapy.
ASJC Scopus subject areas
- Cancer Research