ArticleBMC immunology2011
Transition of tumor-associated macrophages from MHC class II(hi) to MHC class II(low) mediates tumor progression in mice.
Article in BMC immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers, 1 of them a synthesis that pooled it.
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Who cites it
107 citing papers in PubMed, 1 synthesis or guideline pooled it, 152 citations in OpenAlex.
- Pooled it
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- d-serine as a metabolic immune checkpoint in the tumour microenvironment.EBioMedicine · 2026Article
- Tumor implantation site dictates the immune landscape of syngeneic mouse models of head and neck cancer.Scientific reports · 2026Article
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- Local gene editing of fibroblasts in tumors reveals a new cancer-associated fibroblast state.The Journal of experimental medicine · 2026Article
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- Therapeutic targeting of RAGE/STAT3 signaling abrogates S100A7-driven breast tumorigenicity and immune suppression.Breast cancer research : BCR · 2026Article
- HIF-1αImmunity · 2026Article
- Signalling pathways in hepatocellular carcinoma (HCC) metastasis and invasion: Molecular mechanisms and therapeutic implications.Biochemistry and biophysics reports · 2026Review
- Deficiency of lysosomal TMEM175 in myeloid macrophages exerts anti-tumor immunity via inflammasome and cross-presentation pathway.Nature communications · 2026Article
- Beyond density: mapping the functional landscapes of macrophage-T lymphocyte niches in the tumor microenvironment.Frontiers in immunology · 2026Review
- Hypoxic tumor microenvironment and immune cell dynamics: From metabolic reprogramming to therapeutic innovation.Iranian journal of basic medical sciences · 2026Review
- Macrophages in Colorectal Cancer: from Normal Mucosa to Distant Metastasis: Beyond the M1/M2 Paradigm.Journal of Cancer · 2026Review
- Absence of BCAP in myeloid cells abrogates M2 macrophage differentiation and promotes anti-tumor immunity.iScience · 2025Article
- Inhibition of Glutamine Metabolism Attenuates Tumor Progression Through Remodeling of the Macrophage Immune Microenvironment.Advanced biology · 2025Article
- In Vivo Labeling Resolves Distinct Temporal, Spatial, and Functional Properties of Tumor Macrophages and Identifies Subset-Specific Effects of PD-L1 Blockade.Cancer immunology research · 2025Article
- Discovery of a Linked Constellation of Gene Expression Revealed by Local Editing of Fibroblasts in Tumors.bioRxiv : the preprint server for biology · 2025Article
- FOLR2Cell communication and signaling : CCS · 2025Review
- Global research trends in tumor-associated macrophage studies: a bibliometric analysis.Discover oncology · 2025Article
47 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTumor-associated macrophages (TAMs) are the most abundant immune cells within the tumor stroma and play a crucial role in tumor development. Although clinical investigations indicate that high levels of macrophage (MΦ) infiltration into tumors are associated with a poor prognosis, the exact role played by TAMs during tumor development remains unclear. The present study aimed to investigate dynamic changes in TAM major histocompatibility complex (MHC) class II expression levels and to assess the effects of these changes on tumor progression.
resultsSignificant inhibition of tumor growth in the murine hepatocellular carcinoma Hepa1-6 model was closely associated with partial TAM depletion. Strikingly, two distinct TAM subsets were found to coexist within the tumor microenvironment during Hepa1-6 tumor development. An MHC class II(hi) TAM population appeared during the early phase of tumor development and was associated with tumor suppression; however, an MHC class II(low) TAM population became increasingly predominant as the tumor progressed.
conclusionsTumor progression was positively correlated with increasing infiltration of the tumor tissues by MHC class II(low) TAMs. Thus, targeting the transition of MΦ may be a novel strategy for drug development and immunotherapy.
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