TIM-3 blockade reverses oncolytic vaccinia virus-induced DCs inactivation and T cells exhaustion to improve antitumor immunity and therapeutic efficacy.
Peipei Ye, Yi Wu, Xue Yang, Hui Wu, Yongming Xia, Gongqiang Wu, Gang Cheng, Weidong Sun, Junyu Zhang, Shibing Wang, Xiangmin Tong
Abstract
Open AccessOncolytic vaccinia viruses (OVV) demonstrate the capacity to inflame the tumor microenvironment (TME) and elicit infiltrating tumor-specific T cells responses. However, OVV treatment paradoxically alters the cancer-immune equilibrium within tumors, attenuating anti-tumor immunity and necessitating a deeper understanding of the viral-induced immune landscape to optimize therapeutic potential. This study investigates the impact of single-domain antibody-armed OVs targeting TIM-3 on TME remodeling, aiming to overcome localized immunosuppression and enhance tumor responsiveness to immunotherapeutic interventions. We engineered a tumor-selective OVV vector encoding single-domain antibodies against murine (mNbTIM3) or human (hNbTIM3) TIM-3. The therapeutic efficacy of OVV-mNbTIM3 was evaluated across multiple murine cancer models, demonstrating that localized VHHTIM3 delivery via OVV-mNbTIM3 promotes systemic anti-tumor immunity in established cancers. Mechanistically, OVV-mNbTIM3 treatment enhances DCs maturation and tumor-specific CD8+ T cells activation. Notably, intratumoral expression of hNbTIM3 also conferred therapeutic benefit in humanized mice bearing patient-derived cancer xenografts. These findings provide mechanistic insights for enhancing OVV combination therapies and inform the rational design of next-generation oncolytic viruses with engineered immunomodulatory properties.