| First Author | Lim J | Year | 2024 |
| Journal | iScience | Volume | 27 |
| Issue | 9 | Pages | 110810 |
| PubMed ID | 39286510 | Mgi Jnum | J:354292 |
| Mgi Id | MGI:7732866 | Doi | 10.1016/j.isci.2024.110810 |
| Citation | Lim J, et al. (2024) Type I interferon signaling regulates myeloid and T cell crosstalk in the glioblastoma tumor microenvironment. iScience 27(9):110810 |
| abstractText | Downstream interferon signaling through the type I interferon (IFN) receptor, IFNAR, is crucial for the proper production of type I IFNs in mounting anti-tumor immune responses. Our study investigates the role of type I IFN signaling in the glioblastoma (GBM) tumor microenvironment by leveraging single-cell RNA sequencing to analyze tumor-infiltrating lymphocytes. We investigate how type I IFN signaling within the myeloid compartment contributes to the crosstalk with T cells in the tumor microenvironment. Through the use of the Gl261 murine GBM model, we find that the lack of proper type I IFN response results in enhanced PD-L1 interactions among myeloid cells, thereby affecting T cell functionality. Additionally, we also characterize how anti-PD1 treatment induces transcriptional changes in tumor-associated monocytes and macrophages by analyzing intercellular communication networks and propose how immune checkpoint blockade therapy could possibly relieve some of the immunosuppression derived from the lack of proper type I IFN production. |
