ArticleMolecular cancer2026
Therapeutic reprogramming of tumour-associated macrophages in pancreatic cancer using a cytotoxic CCR2-targeted nanotheranostic.
Article in Molecular cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Myeloid-derived suppressor cells in cancer: biology, regulatory networks and theranostic prospects.Signal transduction and targeted therapy · 2026Review
- Rewiring metabolic-immune circuitry in pancreatic ductal adenocarcinoma (PDAC).Cancer pathogenesis and therapy · 2026Article
- Tissue-Resident Macrophage in Inflammation and Cancer.MedComm · 2026Review
- KRAS-driven cytokine-metabolic crosstalk shapes immune exclusion in pancreatic ductal adenocarcinoma.Frontiers in genetics · 2026Review
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Authors and funding
17 authors.
Funding
Abstract
backgroundPancreatic ductal adenocarcinoma (PDAC) exhibits a profoundly immunosuppressive tumour microenvironment (TME) dominated by inflammatory monocytes (IMs) and tumour-associated macrophages (TAMs), which restrict adaptive immunity and drive resistance to immune checkpoint blockade (ICB). Recruitment of CCR2⁺ IMs by tumour-derived CCL2 is a central mechanism underlying TAM accumulation. Conventional gemcitabine (GEM) and small-molecule CCR2 inhibitors provide limited benefit due to poor intratumoural delivery, transient target engagement, and compensatory myeloid recruitment.
methodsWe engineered a CCR2-targeted nanotheranostic by conjugating a CCR2-binding peptide (ECL1i) and GEM onto ultrasmall copper nanoclusters (CuNCs-ECL1i-GEM; C-E-G). Therapeutic efficacy and immune remodelling were evaluated using orthotopic subcutaneous and the autochthonous PDAC mouse models model, using scRNAseq, flow cytometry, multiplex immunohistochemistry, and in vitro functional assays.
resultsC-E-G exhibited robust tumour accumulation and selectively eliminated CCR2⁺ TAMs without systemic myelotoxicity, while durably reprogramming residual macrophages. Mechanistically, C-E-G induced the emergence of an immunostimulatory CCRL2⁺ TAM subset through true macrophage repolarization rather than monocyte replacement. CCRL2⁺ TAMs accumulated intratumoural chemerin, upregulated antigen-presentation and co-stimulatory programs, and were essential for CD8⁺ T-cell recruitment and activation. Genetic and orthotopic studies confirmed their CCR2-independent origin and requirement for tumour control. C-E-G remodelled the TME toward a lymphocyte-permissive inflammatory state and synergized with ICB to induce complete tumour regression and prolong survival in KPPC mice.
conclusionsCCR2-targeted cytotoxic nanotherapy eliminates immunosuppressive CCR2 + TAMs, reprograms the macrophage landscape including CCRL2⁺ TAMs, and unlocks durable anti-tumour immunity in PDAC, supporting translational development of this strategy.
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