Figure 7. Glut1 deletion in neutrophils increases radiotherapy efficacy.

A) μCT analysis of control or Glut1^KO tumors before and after 11.6 Gy radiotherapy (RT) or untreated (mean ± s.e.m.), normalized to the first volume (set to 1) of the same tumors. The tumors’ progression or regression are detailed at 14 days (lower left, n= 17, 13, 12 and 24) and 28 days (lower right, n=17, 13, 11 and 22) after radiotherapy (mean ± s.e.m.). The green line indicates a growth of 1 and numbers indicate the number of tumors with a reduced volume. B) Model illustrating the findings from this study. In the tumor, two neutrophil subpopulations exist. The young Glut3^high anti-tumor neutrophils are recruited by chemoattractants secreted by the non-immune fraction of the tumor, presumably tumor cells. Within the tumor, neutrophils become dependent on Glut1 to survive and to support on-site aging and differentiation. This extensive survival forms a second subpopulation of neutrophils expressing SiglecF and exhibiting tumor-supportive properties. These old neutrophils limit chemoattractant production by tumor cells, thus inhibiting the recruitment of young neutrophils.