ArticleCell reports. Medicine2025
Fc-optimized anti-CTLA-4 antibodies increase tumor-associated high endothelial venules and sensitize refractory tumors to PD-1 blockade.
Article in Cell reports. Medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- High Endothelial Venules in Small Cell Lung Cancer: Prognostic Subtypes and Therapeutic Implications for Immunoradiotherapy.International journal of cancer · 2026Article
- Review
- Synergistic effects of radiotherapy and immunotherapy: improving oncological outcomes.Frontiers in immunology · 2026Review
- TME remodeling and clinical challenges of immune checkpoint blockade in nasopharyngeal carcinoma.Frontiers in oncology · 2026Review
- Clinical and prognostic significance of high-endothelial venule density in regional lymph nodes of esophageal adenocarcinoma.Frontiers in oncology · 2026Article
- Immune Checkpoint Restoration as a Therapeutic Strategy to Halt Diabetes-Driven Atherosclerosis.Biology · 2025Review
- Targeting high endothelial venules: potential strategies for cancer treatment.Annals of medicine · 2025Review
- Endothelial cells as targets of immune checkpoint blockade.Journal for immunotherapy of cancer · 2025Review
- Progressively exploring and assessing the prognosis of bladder urothelial cancer based on the microenvironment through the integration of multiple databases.Frontiers in molecular biosciences · 2025Article
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
The lack of T cells in tumors is a major hurdle to successful immune checkpoint therapy (ICT). Therefore, therapeutic strategies promoting T cell recruitment into tumors are warranted to improve the treatment efficacy. Here, we report that Fc-optimized anti-cytotoxic T lymphocyte antigen 4 (CTLA-4) antibodies are potent remodelers of tumor vasculature that increase tumor-associated high endothelial venules (TA-HEVs), specialized blood vessels supporting lymphocyte entry into tumors. Mechanistically, this effect is dependent on the Fc domain of anti-CTLA-4 antibodies and CD4
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Registered trials
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