ArticleImmunity2022
Tumor-associated macrophages expressing the transcription factor IRF8 promote T cell exhaustion in cancer.
Article in Immunity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 130 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
130 citing papers in PubMed, 174 citations in OpenAlex.
- Analysis of PD1, LAG3, TIGIT, and TIM3 expression in human lung adenocarcinoma reveals a 25-gene signature predicting immunotherapy response.Cell reports. Medicine · 2024Trial
- Early Immune Remodeling Steers Clinical Response to First-Line Chemoimmunotherapy in Advanced Gastric Cancer.Cancer discovery · 2024Trial
- Interferon regulatory factors orchestrate CD8International journal of molecular medicine · 2026Review
- IRF8 Suppresses Hepatocellular Carcinoma Progression Through LIAS-Dependent IFN Production and Cuproptosis Activation.Genes, chromosomes & cancer · 2026Article
- Pathophysiological roles of monocytes and macrophages in cancer.Nature reviews. Immunology · 2026Review
- d-serine as a metabolic immune checkpoint in the tumour microenvironment.EBioMedicine · 2026Article
- Hypoxia shapes both therapeutic response and resistance in metastatic clear cell renal cell carcinoma.Cancer cell · 2026Article
- Imaging mass cytometry reveals functional and immunological changes during type 1 diabetes progression in human pancreata.Nature metabolism · 2026Article
- Transcription factors remodel tumor immune microenvironment by impacting multiple immune cells.Discover oncology · 2026Review
- Programming the immunological properties of mRNA vaccines for cancer.Nature reviews. Immunology · 2026Review
- NF-κB-activated fibroblasts orchestrate inflammaging and emergence of pro-inflammatory granzyme KImmunity · 2026Article
- Explainable machine learning-guided integrated multiomics analysis reveals macrophage-driven immune suppression in breast cancer.Nature communications · 2026Article
- CKS1B is a tumor-intrinsic factor driving CD8Science advances · 2026Article
- Targeting caveolin-1: dual challenges in tumor immunity and drug therapy strategies.Cancer cell international · 2026Review
- Identification and validation of an intratumor heterogeneity-related prognostic signature in triple-negative breast cancer: a study based on integrative machine learning and single-cell sequencing.Breast cancer research : BCR · 2026Article
- Upregulation of TNFR2 Precedes TOX Expression by Exhausted T cells and Restricts Antitumor and Antiviral Immunity.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026Article
- mRNA vaccines in cancer immunotherapy: current progress and perspectives in solid tumors and hematologic malignancies.MedScience · 2026Review
- Leveraging glucan-induced trained immunity for the epigenetic and metabolic rewiring of macrophages to enhance colorectal cancer vaccine response.Nature communications · 2026Article
- Integrative Multi-Omics Analysis Reveals Molecular Signatures of Recurrence in Paired Primary and Recurrent High-Grade Serous Ovarian Cancer.International journal of molecular sciences · 2026Article
- Targeting innate immunity in cancer: mechanistic foundations, therapeutic vaccination, and clinical translation.Frontiers in immunology · 2026Review
70 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
22 authors at 4 institutions in 1 country.
Funding
Abstract
Tumors are populated by antigen-presenting cells (APCs) including macrophage subsets with distinct origins and functions. Here, we examined how cancer impacts mononuclear phagocytic APCs in a murine model of breast cancer. Tumors induced the expansion of monocyte-derived tumor-associated macrophages (TAMs) and the activation of type 1 dendritic cells (DC1s), both of which expressed and required the transcription factor interferon regulatory factor-8 (IRF8). Although DC1s mediated cytotoxic T lymphocyte (CTL) priming in tumor-draining lymph nodes, TAMs promoted CTL exhaustion in the tumor, and IRF8 was required for TAMs' ability to present cancer cell antigens. TAM-specific IRF8 deletion prevented exhaustion of cancer-cell-reactive CTLs and suppressed tumor growth. Tumors from patients with immune-infiltrated renal cell carcinoma had abundant TAMs that expressed IRF8 and were enriched for an IRF8 gene expression signature. Furthermore, the TAM-IRF8 signature co-segregated with CTL exhaustion signatures across multiple cancer types. Thus, CTL exhaustion is promoted by TAMs via IRF8.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.