| First Author | Banerjee H | Year | 2021 |
| Journal | Cell Rep | Volume | 36 |
| Issue | 11 | Pages | 109699 |
| PubMed ID | 34525351 | Mgi Jnum | J:321210 |
| Mgi Id | MGI:6876886 | Doi | 10.1016/j.celrep.2021.109699 |
| Citation | Banerjee H, et al. (2021) Expression of Tim-3 drives phenotypic and functional changes in Treg cells in secondary lymphoid organs and the tumor microenvironment. Cell Rep 36(11):109699 |
| abstractText | Regulatory T cells (Treg cells) are critical mediators of self-tolerance, but they can also limit effective anti-tumor immunity. Although under homeostasis a small fraction of Treg cells in lymphoid organs express the putative checkpoint molecule Tim-3, this protein is expressed by a much larger proportion of tumor-infiltrating Treg cells. Using a mouse model that drives cell-type-specific inducible Tim-3 expression, we show that expression of Tim-3 by Treg cells is sufficient to drive Treg cells to a more effector-like phenotype, resulting in increases in suppressive activity, effector T cell exhaustion, and tumor growth. We also show that T-reg-cell-specific inducible deletion of Tim-3 enhances anti-tumor immunity. Enhancement of Treg cell function by Tim-3 is strongly correlated with increased expression of interleukin-10 (IL-10) and a shift to a more glycolytic metabolic phenotype. Our data demonstrate that Tim-3(+) Treg cells may be a relevant therapeutic target cell type for the treatment of cancer. |
