GSE201557
CD169 is a marker of IFN-?-stimulated inflammatory macrophages in brain tumor [EGFRviii]
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 genetically engineered GBM samples, deletion of PTEN and TP53, and overexpression of EGFRviii were induced in mouse brain ventricle. 16 weeks later, immune cells (CD45+) were sorted from brain tumor and normal brain and analyzed.