GSE201553
CD169 is a marker of IFN-?-stimulated inflammatory macrophages in brain tumor [CT2A]
Therapies against glioblastoma multiforme (GBM) have been largely ineffective due to the infiltration of immunosuppressive tumor-associated macrophages (TAMs). Recent studies demonstrated that TAMs can also be immune-activating. However, markers differentiating these heterogeneous macrophage populations have not been established. In this study, we identified a subset of macrophages expressing CD169 that promote an anti-tumoral microenvironment in GBM. Using single-cell transcriptome analysis, we found that CD169+ macrophages in human and mouse gliomas produced proinflammatory chemokines, leading to the accumulation of T cells and NK cells. Depletion of CD169+ macrophages shortened the survival of mice with gliomas and reduced the function of antitumor lymphocytes. We show that IFN-? produced by NK cells was critical for the accumulation of CD169+ macrophages into gliomas. Additionally, CD169 expression on macrophages increased the phagocytosis of apoptotic glioma cells. Our finding suggests that the CD169+ subset of TAMs promotes antitumor immune responses against GBM. Overall design: We analyzed glioma infiltrated immune cells by single cell RNA sequencing (scRNAseq) with 10X genomics.   For CT2A tumor in C57BL/6 WT mice, mice were injected with 100000 tumor cells. CD45.2+ immune cells were sorted from brain tumors and analyzed at 10 dpi.