ArticleACS central science2025
Targeting Sialidase to PD1 Enhances T cell Function and Tumor Control.
Article in ACS central science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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The trial behind it
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
10 citing papers in PubMed.
- Biomaterial engineering of the tumor glycocalyx for cancer immunotherapy.Materials today. Bio · 2026Review
- Targeting Siglec-engaging immunosuppressive sialoglycans to suppress prostate cancer bone metastasis.British journal of cancer · 2026Article
- Enzyme-mediated remodeling of the extracellular matrix and glycocalyx to enhance immunotherapy in solid tumors.Bioengineering & translational medicine · 2026Review
- Impact of sialyltransferase deletion in mature T cells on control of subcutaneous and metastatic cancers.Glycobiology · 2026Article
- Chemically Masked aPD-L1-Sialidase Conjugate for Tumor-Specific Desialylation and Immunotherapy.Angewandte Chemie (International ed. in English) · 2026Article
- Immune implications and therapeutic opportunities of tumor glycosylation.Nature cancer · 2026Review
- Engineering Extracellular Vesicles for Anti-Aging Therapy: Mechanisms, Applications, and Perspectives.Aging cell · 2026Review
- Writers and readers of sialylation in immunoregulation in cancer.The Journal of biological chemistry · 2026Review
- Glycomic Insights in Gynecological Disease: From Molecular Mechanisms to Precision Diagnostics and Therapeutics.International journal of molecular sciences · 2026Review
- Network Pharmacology and Transcriptomic Analysis Reveal the Therapeutic Mechanisms of Xiebai Bining Decoction in Hyperuricemic Nephropathy.Combinatorial chemistry & high throughput screening · 2026Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Immune therapies targeting the PD1 axis have transformed outcomes in cancer treatment by enhancing T cell-mediated immune responses. However, many tumors evade immune clearance through orthogonal escape mechanisms. Excessive production of immunosuppressive sialic acid-containing glycans (sialoglycans) can impair immune surveillance by recruiting inhibitory Siglecs to the immune synapse where, like PD1, they act as checkpoints for cell activation. Sialic acids can also impact T cell activation by dampening the ligation of the costimulatory receptor CD28 with its ligands. This polypharmacology implicates sialoglycans as a linchpin of tumor immunity that can be targeted to further improve outcomes of PD1 therapies. In this work we conjugated sialidase to anti-PD1 (αPD1-S) to selectively degrade sialic acids on immune cells expressing PD1. Glycan profiling confirmed targeted desialylation, and functional assays demonstrated enhancements to T cell activation and cytotoxic capacity. In a melanoma model, αPD1-S promoted inflammatory macrophage polarization and reduced T cell exhaustion, collectively restricting melanoma growth beyond anti-PD1 (αPD1) alone. By simultaneously blocking PD1 and degrading sialoglycans, αPD1-S provides a novel strategy to enhance T cell-mediated immune responses and improve tumor control in refractory cancers.
Identifiers
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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.