ArticleCancer immunology research2014
Tumoral immune suppression by macrophages expressing fibroblast activation protein-α and heme oxygenase-1.
Article in Cancer immunology research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers.
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Who cites it
117 citing papers in PubMed, 166 citations in OpenAlex.
- Unraveling the roles of fibroblast activation protein‑positive cancer‑associated fibroblasts in cancer: From mechanisms to therapy (Review).International journal of oncology · 2026Review
- Aggressive breast cancers secrete heme metabolites to alter macrophage immune suppression and function.Communications biology · 2026Article
- The pro-cancer and immunosuppressive activity of macrophage-transformed cancer-associated fibroblasts in oral squamous cell carcinoma.Journal of advanced research · 2026Article
- FAPαAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Cancer-associated fibroblasts: enablers of tumor drug resistance.Journal of translational medicine · 2026Review
- Gasotransmitters bridging tumor biology and immunity: from pathophysiological insights to therapeutic potential.Frontiers in immunology · 2026Review
- Analysis of the expression of FAP, Caveolin1, and CPXM2 and prognostic significance in gastric cancer.Frontiers in oncology · 2026Article
- Cancer-Associated Fibroblasts in Prostate Cancer: Unraveling Mechanisms and Therapeutic Implications.Oncology research · 2026Review
- Unraveling the impact of cancer-associated fibroblasts on lymphatic metastasis of head and neck squamous cell carcinoma.Cellular oncology (Dordrecht, Netherlands) · 2025Review
- Different detection rates of brain metastasis in different pathological types of lung cancer byBMC cancer · 2025Article
- Identification ofCancers · 2025Article
- Tumor microenvironments with an active type I IFN response are sensitive to inhibitors of heme degradation.JCI insight · 2025Article
- An oral heme oxygenase inhibitor targets immunosuppressive perivascular macrophages in preclinical models of cancer.Science translational medicine · 2025Article
- Stromal Cells in Early Inflammation-Related Pancreatic Carcinogenesis-Biology and Its Potential Role in Therapeutic Targeting.Cancers · 2025Review
- Article
- Synergistic effects of HO-1 inhibition and chemotherapy on tumor proliferation and immune infiltration: An in vitro and in vivo approach to enhancing prostate cancer treatment.Translational oncology · 2025Article
- The multi-faceted roles of cancer-associated fibroblasts in pancreatic cancer.Cellular signalling · 2025Review
- Fibroblast activation protein and the tumour microenvironment: challenges and therapeutic opportunities.Oncology reviews · 2025Review
- The implications of oncolytic viruses targeting fibroblasts in enhancing the antitumoural immune response.Heliyon · 2024Review
- The BRD4 Inhibitor I-BET-762 Reduces HO-1 Expression in Macrophages and the Pancreas of Mice.International journal of molecular sciences · 2024Article
57 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The depletion of tumor stromal cells that are marked by their expression of the membrane protein fibroblast activation protein-α (FAP) overcomes immune suppression and allows an anticancer cell immune response to control tumor growth. In subcutaneous tumors established with immunogenic Lewis lung carcinoma cells expressing ovalbumin (LL2/OVA), the FAP(+) population is comprised of CD45(+) and CD45(-) cells. In the present study, we further characterize the tumoral FAP(+)/CD45(+) population as a minor subpopulation of F4/80(hi)/CCR2(+)/CD206(+) M2 macrophages. Using bone marrow chimeric mice in which the primate diphtheria toxin receptor is restricted either to the FAP(+)/CD45(+) or to the FAP(+)/CD45(-) subset, we demonstrate by conditionally depleting each subset that both independently contribute to the immune-suppressive tumor microenvironment. A basis for the function of the FAP(+)/CD45(+) subset is shown to be the immune inhibitory enzyme, heme oxygenase-1 (HO-1). The FAP(+)/CD45(+) cells are the major tumoral source of HO-1, and an inhibitor of HO-1, Sn mesoporphyrin, causes the same extent of immune-dependent arrest of LL2/OVA tumor growth as does the depletion of these cells. Because this observation of immune suppression by HO-1 expressed by the FAP(+)/CD45(+) stromal cell is replicated in a transplanted model of pancreatic ductal adenocarcinoma, we conclude that pharmacologically targeting this enzyme may improve cancer immunotherapy.
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