| First Author | Yang X | Year | 2014 |
| Journal | Cancer Cell | Volume | 25 |
| Issue | 1 | Pages | 37-48 |
| PubMed ID | 24434209 | Mgi Jnum | J:208155 |
| Mgi Id | MGI:5561177 | Doi | 10.1016/j.ccr.2013.12.004 |
| Citation | Yang X, et al. (2014) Targeting the tumor microenvironment with interferon-beta bridges innate and adaptive immune responses. Cancer Cell 25(1):37-48 |
| abstractText | Antibodies (Abs) that preferentially target oncogenic receptors have been increasingly used for cancer therapy, but tumors often acquire intrinsic Ab resistance after prolonged and costly treatment. Herein we armed the Ab with IFNbeta and observed that it is more potent than the first generation of Ab for controlling Ab-resistant tumors. This strategy controls Ab resistance by rebridging suppressed innate and adaptive immunity in the tumor microenvironment. Mechanistically, Ab-IFNbeta therapy primarily and directly targets intratumoral dendritic cells, which reactivate CTL by increasing antigen cross-presentation within the tumor microenvironment. Additionally, blocking PD-L1, which is induced by Ab-IFNbeta treatment, overcomes treatment-acquired resistance and completely eradicates established tumors. This study establishes a next-generation Ab-based immunotherapy that targets and eradicates established Ab-resistant tumors. |
