ArticleCancer research2025
Scavenger Receptor CD36 in Tumor-Associated Macrophages Promotes Cancer Progression by Dampening Type-I IFN Signaling.
Article in Cancer research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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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
20 citing papers in PubMed.
- Lipid metabolic reprogramming of tumor-associated macrophages drives resistance to immune checkpoint blockade in lung cancer: a narrative review of mechanisms and therapeutic strategies.Translational lung cancer research · 2026Review
- CD36 as a Context-Dependent Regulator of Metabolic Switching in Acute and Chronic Hypoxia.Biomolecules · 2026Review
- Heritable single-cell gene expression states shape functional variability in innate immune responses.bioRxiv : the preprint server for biology · 2026Article
- Article
- Metabolic regulation of tumor-associated macrophage function and immunotherapy in cancer.Cancer biology & medicine · 2026Review
- Multi-omics profiling identifies ectopic olfactory receptors as putative drivers of tumor progression and prognostic indicators in clear cell renal cell carcinoma.Clinical and experimental medicine · 2026Article
- Review
- CD36 as a potential prognostic biomarker and modulator of the tumor microenvironment in glioma.Translational cancer research · 2026Article
- The Role of Low CD36 Expression in the Development of Non-Small Cell Lung Cancer and Its Potential for Therapy.Cancers · 2026Review
- Label-free quantitative urinary proteomics for non-invasive biomarker discovery in endometrial cancer.Frontiers in medicine · 2026Article
- CD36 in asthma: from a candidate immunometabolic checkpoint to genetic susceptibility.Frontiers in immunology · 2026Review
- Lipid metabolic reprogramming in clear cell renal cell carcinoma: focus on high-density lipoprotein-related pathways.Oncology reviews · 2026Review
- Increased expression of CD36 and CD163 in clear cell renal cell carcinoma suggests an association between lipid transport and an "M2-like" macrophage phenotype.Frontiers in immunology · 2026Article
- Metabolic symbiosis and competition: the dual nature of TAM-tumor cell cross-talk in tumor progression.Frontiers in oncology · 2026Review
- Tumor-associated macrophages in cancer: from mechanisms to application.Molecular biomedicine · 2025Review
- Role of oxygen sensing and hypoxia-inducible factors in orchestrating innate immune responses.Nature immunology · 2025Review
- Immunometabolism: crosstalk with tumor metabolism and implications for cancer immunotherapy.Molecular cancer · 2025Review
- Near-infrared fatty acid molecular probe for image-guided surgery of glioblastoma.Npj imaging · 2025Article
- Single-cell profiling uncovers the intricate pathological niche diversity in brain, lymph node, bone, and adrenal metastases of lung cancer.Discover oncology · 2025Article
- Lipid metabolic reprogramming in the tumor microenvironment and its mechanistic role in immunosuppressive cells.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Tumor-associated macrophages (TAM) are a heterogeneous population of myeloid cells that dictate the inflammatory tone of the tumor microenvironment. In this study, we unveiled a mechanism by which scavenger receptor cluster of differentiation 36 (CD36) suppresses TAM inflammatory states. CD36 was upregulated in TAMs and associated with immunosuppressive features, and myeloid-specific deletion of CD36 significantly reduced tumor growth. Moreover, CD36-deficient TAMs acquired inflammatory signatures including elevated type-I IFN (IFNI) production, mirroring the inverse correlation between CD36 and IFNI response observed in patients with cancer. IFNI, especially IFNβ, produced by CD36-deficient TAMs directly induced tumor cell quiescence and delayed tumor growth. Mechanistically, CD36 acted as a natural suppressor of IFNI signaling in macrophages through p38 activation downstream of oxidized lipid signaling. These findings establish CD36 as a critical regulator of TAM function and the tumor inflammatory microenvironment, providing additional rationale for pharmacologic inhibition of CD36 to rejuvenate antitumor immunity. Significance: CD36 in tumor-associated macrophages mediates immunosuppression and can be targeted as a therapeutic avenue for stimulating interferon production and increasing the efficacy of immunotherapy.
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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.