Oncolytic herpes simplex virus<scp>HF10</scp>(canerpaturev) promotes accumulation of<scp>CD8</scp>⁺<scp>PD</scp>‐1⁻tumor‐infiltrating T cells in<scp>PD‐L1</scp>‐enriched tumor microenvironment

Oncolytic viruses (OVs) remodel the tumor microenvironment by switching a “cold” into “hot” with high CD8+ T-cell infiltration. activity plays an essential role in antitumor efficacy of OVs. However, T cells is impaired programmed cell death protein-1/programmed death-ligand 1 (PD-1/PD-L1) interaction. To date, it remains unclear why OVs alone have significant even when PD-L1 expression persists on or immune cells. In this study, we found that canerpaturev (C-REV) treatment significantly suppressed growth, though induced increase tumors vivo as well persistence antigen-presenting (macrophage and dendritic [DCs]). Surprisingly, observed C-REV increased abundance activated CD8+PD-1− tumor-infiltrating lymphocytes (TILs) both injected contralateral sides, although infiltration CD8+PD-1high TILs was control group. Moreover, difference PD-1 only after C-REV, whereas most spleen, tumor-draining lymph nodes blood were PD-1-negative, did not change treatment. addition, changes immunoglobulin mucin-domain containing-3 immune-receptor Ig ITIM domains Taken together, our findings may reveal mechanisms allow to trigger response, irrespective PD-L1-enriched microenvironment, recruitment TILs.