“Ter” cells (officially CD45-Ter119+CD71+ erythroid progenitor cells), precursors to certain types of blood cells, are induced in the spleen by tumors and are thought to promote tumor progression by secreting a factor known as artemin. Now a study led by Ludwig Chicago’s Ralph Weichselbaum and Yang-Xin Fu of the University of Texas Southwestern Medical Center has found that both targeted radiotherapy and anti-PD-L1 immunotherapy deplete Ter cells in the spleens of mouse models and reduce artemin levels outside the field of radiation. The researchers reported in a February paper in Science Translational Medicine that Ter cell depletion or the blockade of artemin or its signaling partners boosted the therapeutic effects of both IR and anti-PD-L1 immunotherapy against various tumor types. That effect was mediated by killer T cells, which target cancer cells, and the production of interferon-γ, an immune-stimulating factor. Conversely, giving mice erythropoietin—which promotes Ter cell proliferation—induced resistance to those therapies. An examination of samples from patients with melanoma who had received immunotherapy or patients with lung cancer who received radiotherapy demonstrated that favorable responses were associated with a reduction of Ter cells, artemin or its signaling partners. The researchers note that their study identified several potential drug targets to improve outcomes of radiotherapy and immunotherapy.
This article appeared in the August 2021 issue of Ludwig Link. Click here to download a PDF (2MB).