Triple targeting of STING, TGF-β, and PD-L1 boosts CXCL16-CXCR6 signaling for potent antitumor response - PubMed
3 months ago
- #immunotherapy
- #cancer research
- #immune checkpoint
- Triple targeting of STING, TGF-β, and PD-L1 enhances CXCL16-CXCR6 signaling for antitumor response.
- TGF-β×PD-L1 bispecific antibody (BsAb) efficacy is limited by insufficient innate immune activation.
- Combining STING agonists with BsAb improves tumor suppression beyond standard STING agonist plus anti-PD-L1 combinations.
- TGF-β blockade enhances STING agonist monotherapy, indicating TGF-β suppresses STING-driven immune activation.
- Synergy is mediated by the CXCL16-CXCR6 axis, promoting cytotoxic T cell recruitment and activity.
- PD-L1 blockade further boosts antitumor effects of the CXCL16-CXCR6 axis.
- Y101S, an antibody-drug conjugate targeting TGF-β, PD-L1, and STING, shows superior tumor control in preclinical models.