ArticleThe Journal of experimental medicine2024
ICOS costimulation in combination with CTLA-4 blockade remodels tumor-associated macrophages toward an antitumor phenotype.
Article in The Journal of experimental medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 34 citations in OpenAlex.
- B Cells and Tumor Immunometabolism: Emerging Insights into Immune Regulation and Therapeutic Resistance.Antibodies (Basel, Switzerland) · 2026Review
- Harnessing myeloid cell plasticity for cancer therapy.Nature cancer · 2026Review
- A macrophage MHC-I axis links intratumoral heterogeneity to terminal CD8NPJ precision oncology · 2026Article
- miR-155 aberrant expression impairs tumor rejection because of its targeting of ICOSL and multiple pathways implicated in the antitumor response.Pharmacological reviews · 2026Review
- Crosstalk between tumor-associated macrophages and the B7/CD28 family in immune checkpoint inhibitor-induced immunotherapy.Molecular and cellular biochemistry · 2026Review
- Macrophage-Dendritic Cell-T-Cell Tetrads Orchestrate Antitumor Immunity and Response to Checkpoint Blockade.bioRxiv : the preprint server for biology · 2025Article
- CST7Translational cancer research · 2025Article
- Intestinal reengineering: Scientific advances in intestinal transplantation.World journal of gastrointestinal surgery · 2025Review
- Tumor-associated macrophages: untapped molecular targets to improve T cell-based immunotherapy.Molecular cancer · 2025Review
- The costimulatory molecule ICOS limits memory-like properties and function of exhausted PD-1Immunity · 2025Article
- Review
- CyTOF as a suitable tool for stratification and monitoring of cancer patients.Journal of translational medicine · 2025Review
- Fc-optimized anti-CTLA-4 antibodies increase tumor-associated high endothelial venules and sensitize refractory tumors to PD-1 blockade.Cell reports. Medicine · 2025Article
- Tumor-associated macrophages remodel the suppressive tumor immune microenvironment and targeted therapy for immunotherapy.Journal of experimental & clinical cancer research : CR · 2025Review
- Neoadjuvant immune checkpoint therapy: Enabling insights into fundamental human immunology and clinical benefit.Cancer cell · 2025Review
- ICOS-expressing CAR-T cells mediate durable eradication of triple-negative breast cancer and metastasis.Journal for immunotherapy of cancer · 2025Article
- Targeting novel regulated cell death: disulfidptosis in cancer immunotherapy with immune checkpoint inhibitors.Biomarker research · 2025Review
- Recent advances in novel tumor immunotherapy strategies based on regulating the tumor microenvironment and immune checkpoints.Frontiers in immunology · 2025Review
- Targeting tumor-associated macrophages in gastric cancer progression and therapy: insights from molecular mechanisms to therapeutic applications.Frontiers in pharmacology · 2025Review
- Lactylation and antitumor immunity.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
We have previously demonstrated synergy between ICOS costimulation (IVAX; ICOSL-transduced B16-F10 cellular vaccine) and CTLA-4 blockade in antitumor therapy. In this study, we employed CyTOF and single-cell RNA sequencing and observed significant remodeling of the lymphoid and myeloid compartments in combination therapy. Compared with anti-CTLA-4 monotherapy, the combination therapy enriched Th1 CD4 T cells, effector CD8 T cells, and M1-like antitumor proinflammatory macrophages. These macrophages were critical to the therapeutic efficacy of anti-CTLA-4 combined with IVAX or anti-PD-1. Macrophage depletion with clodronate reduced the tumor-infiltrating effector CD4 and CD8 T cells, impairing their antitumor functions. Furthermore, the recruitment and polarization of M1-like macrophages required IFN-γ. Therefore, in this study, we show that there is a positive feedback loop between intratumoral effector T cells and tumor-associated macrophages (TAMs), in which the IFN-γ produced by the T cells polarizes the TAMs into M1-like phenotype, and the TAMs, in turn, reshape the tumor microenvironment to facilitate T cell infiltration, immune function, and tumor rejection.
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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.