ArticleProceedings of the National Academy of Sciences of the United States of America2005
Evolutionarily divergent herpesviruses modulate T cell activation by targeting the herpesvirus entry mediator cosignaling pathway.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
114 citing papers in PubMed, 203 citations in OpenAlex.
- Human Cytomegalovirus Genetic Diversity, Clinical Relevance, and Emerging Insights.Reviews in medical virology · 2026Review
- PD-1, BTLA and TIGIT as therapeutic targets for rheumatic disease.Nature reviews. Rheumatology · 2026Review
- Auguries of adaptivity: LES γδ TCR ligand recognition revisited.Trends in immunology · 2026Review
- MutantFrontiers in immunology · 2026Article
- Unlocking new frontiers: novel immune targets for next-generation cancer immunotherapy.Korean journal of clinical oncology · 2025Review
- Quantitative detection of the HVEM-BTLA checkpoint receptor cis-complex in human lymphocytes.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Cognitive Impact of Neurotropic Pathogens: Investigating Molecular Mimicry through Computational Methods.Cellular and molecular neurobiology · 2024Article
- Multilayered Computational Framework for Designing Peptide Inhibitors of HVEM-LIGHT Interaction.The journal of physical chemistry. B · 2024Article
- Soluble immune checkpoints: implications for cancer prognosis and response to immune checkpoint therapy and conventional therapies.Journal of experimental & clinical cancer research : CR · 2024Review
- The role of the BTLA-HVEM complex in the pathogenesis of breast cancer.Breast cancer (Tokyo, Japan) · 2024Review
- BTLA biology in cancer: from bench discoveries to clinical potentials.Biomarker research · 2024Review
- The effect of gD-derived peptides on T cell immune response mediated by BTLA-HVEM protein complex in melanoma patients.Frontiers in immunology · 2024Article
- ADAM17 targeting by human cytomegalovirus remodels the cell surface proteome to simultaneously regulate multiple immune pathways.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Review
- Epitope topography of agonist antibodies to the checkpoint inhibitory receptor BTLA.Structure (London, England : 1993) · 2023Article
- Deletion of the non-adjacent genesFrontiers in immunology · 2023Article
- Contribution of carbohydrate-related metabolism in Herpesvirus infections.Current research in microbial sciences · 2023Article
- Tumor Cell-Intrinsic BTLA Receptor Inhibits the Proliferation of Tumor Cells via ERK1/2.Cells · 2022Article
- A Novel Multiplexed Enzyme-Linked Immunosorbent Assay for the Detection of IgG Seroreactivity to Cytomegalovirus (CMV) UL144.Journal of clinical microbiology · 2021Article
- Immune Checkpoints, a Novel Class of Therapeutic Targets for Autoimmune Diseases.Frontiers in immunology · 2021Review
54 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 3 institutions in 1 country.
Funding
Abstract
The herpesvirus entry mediator (HVEM), a member of the TNF receptor (TNFR) superfamily, can act as a molecular switch that modulates T cell activation by propagating positive signals from the TNF-related ligand LIGHT (TNFR superfamily 14), or inhibitory signals through the Ig superfamily member B and T lymphocyte attenuator (BTLA). Competitive binding analysis and mutagenesis reveals a unique BTLA binding site centered on a critical lysine residue in cysteine-rich domain 1 of HVEM. The BTLA binding site on HVEM overlaps with the binding site for the herpes simplex virus 1 envelope glycoprotein D, but is distinct from where LIGHT binds, yet glycoprotein D inhibits the binding of both ligands, potentially nullifying the pathway. The binding site on HVEM for BTLA is conserved in the orphan TNFR, UL144, present in human CMV. UL144 binds BTLA, but not LIGHT, and inhibits T cell proliferation, selectively mimicking the inhibitory cosignaling function of HVEM. The demonstration that distinct herpesviruses target the HVEM-BTLA cosignaling pathway suggests the importance of this pathway in regulating T cell activation during host defenses.
Indexed as
Identifiers
What OpenQuestion holds
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.