ArticleNature communications2025
Targeting site-specific N-glycosylated B7H3 induces potent antitumor immunity.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed.
- Molecular Architecture and Clinical Landscape of Immune Checkpoint Receptors and Ligands.Antibodies (Basel, Switzerland) · 2026Review
- Post-translational modifications in metabolic reprogramming: implications for metabolic therapy and immunotherapy in cancer.Signal transduction and targeted therapy · 2026Review
- Review
- Immune implications and therapeutic opportunities of tumor glycosylation.Nature cancer · 2026Review
- Immune Cell Therapy Promises More Effective Cure for Medulloblastoma.Journal of personalized medicine · 2026Review
- Review
- LGALS1-CD276 Paracrine axis between tumor and endothelial cells promotes tumor angiogenesis and progression in bladder cancer.Cell death and differentiation · 2026Article
- Review
- CD276 immature glycosylation drives colorectal cancer aggressiveness and T cell mediated immune escape.Cell communication and signaling : CCS · 2026Article
- Endoplasmic reticulum stress in skeletal muscle dysfunction of type 2 diabetes: mechanisms and therapeutic implications.Frontiers in endocrinology · 2026Review
- The Search for Predictive Biomarkers in Response to Immune Checkpoint Inhibitors and Associated Adverse Events.Journal of personalized medicine · 2025Review
- Therapeutic Targeting of Viral N-Glycosylation Modification: From Molecular Mechanisms to Clinical Application Prospects.Infectious diseases and therapy · 2025Review
- The B7-H3 (CD276) pathway: emerging biology and clinical therapeutics.Trends in pharmacological sciences · 2025Review
Corrections and comments
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Authors and funding
17 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
B7H3, an immune checkpoint molecule, is a highly N-glycosylated membrane protein. However, the key glycosylated asparagine residues that mediate the function of the B7H3 protein are still unclear. Here we identify that N-glycans attached to asparagine residues N91/309 and N104/322 are required for proper B7H3 localization on the cell surface membrane. We demonstrate that mutations in these two pairs of N-glycosylation sites induce ER accumulation of B7H3 by blocking its ER-to-Golgi translocation and subsequently promote its degradation via the endoplasmic reticulum-associated protein degradation pathway. Additional evidence suggests that N-glycosylation at N91/309 and N104/322 of B7H3 is essential for its inhibition of T-cell proliferation and activation. More importantly, a monoclonal antibody, Ab-82, preferentially targeting B7H3 glycosylated at N91/309 and N104/322 is developed, which exhibits the ability to elicit cytotoxic T lymphocyte-mediated antitumor immunity via B7H3 internalization. Together, these findings offer a rationale for targeting glycosylated B7H3 as a potential strategy for immunotherapy.
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