| First Author | Katlinski KV | Year | 2017 |
| Journal | Cancer Cell | Volume | 31 |
| Issue | 2 | Pages | 194-207 |
| PubMed ID | 28196594 | Mgi Jnum | J:239672 |
| Mgi Id | MGI:5829488 | Doi | 10.1016/j.ccell.2017.01.004 |
| Citation | Katlinski KV, et al. (2017) Inactivation of Interferon Receptor Promotes the Establishment of Immune Privileged Tumor Microenvironment. Cancer Cell 31(2):194-207 |
| abstractText | Refractoriness of solid tumors, including colorectal cancers (CRCs), to immunotherapies is attributed to the immunosuppressive tumor microenvironment that protects malignant cells from cytotoxic T lymphocytes (CTLs). We found that downregulation of the type I interferon receptor chain IFNAR1 occurs in human CRC and mouse models of CRC. Downregulation of IFNAR1 in tumor stroma stimulated CRC development and growth, played a key role in formation of the immune-privileged niche, and predicted poor prognosis in human CRC patients. Genetic stabilization of IFNAR1 improved CTL survival and increased the efficacy of the chimeric antigen receptor T cell transfer and PD-1 inhibition. Likewise, pharmacologic stabilization of IFNAR1 suppressed tumor growth providing the rationale for upregulating IFNAR1 to improve anti-cancer therapies. |
