Transcriptional profiling of Cd169-lineage lymph node macrophages
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA883698 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR21684703_1.fastq.gz | Fastqsanger.gz | |||
| SRR21684703_2.fastq.gz | Fastqsanger.gz | |||
| SRR21684704_1.fastq.gz | Fastqsanger.gz | |||
| SRR21684704_2.fastq.gz | Fastqsanger.gz | |||
| SRR21684705_1.fastq.gz | Fastqsanger.gz |
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Project description: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-γ 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.
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