The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.
Evolutionarily divergent herpesviruses modulate T cell activation by targeting the herpesvirus entry mediator cosignaling pathway
Open accessAbstract
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.
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Cites
CTLA-4: new insights into its biological function and use in tumor immunotherapy
Egen, J. G., Kuhns, M. S., & Allison, J. P. (2002) · Nature Immunology · doi:10.1038/ni0702-611 · Cited by 940
BTLA is a lymphocyte inhibitory receptor with similarities to CTLA-4 and PD-1
Watanabe, N., Gavrieli, M., Sedy, J. R., Yang, J., Fallarino, F., Loftin, S. K., Hurchla, M. A., Zimmerman, N., Sim, J., Zang, X., et al. (2003) · Nature Immunology · doi:10.1038/ni944 · Cited by 883
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Cited by
Immune checkpoint signaling and cancer immunotherapy
He, X., & Xu, C. (2020) · Cell Research · doi:10.1038/s41422-020-0343-4 · Cited by 1,371
Balancing co-stimulation and inhibition with BTLA and HVEM
Murphy, K. M., Nelson, C. A., & Šedý, J. R. (2006) · Nature Reviews Immunology · doi:10.1038/nri1917 · Cited by 309
Self-citationThe CD160, BTLA, LIGHT/HVEM pathway: a bidirectional switch regulating T‐cell activation
Cai, G., & Freeman, G. J. (2009) · Immunological Reviews · doi:10.1111/j.1600-065x.2009.00783.x · Cited by 301
Loss of the HVEM Tumor Suppressor in Lymphoma and Restoration by Modified CAR-T Cells
Boice, M., Salloum, D., Mourcin, F., Sanghvi, V., Amin, R., Oricchio, E., Jiang, M., Mottok, A., Denis-Lagache, N., Ciriello, G., et al. (2016) · Cell · doi:10.1016/j.cell.2016.08.032 · Cited by 257
Tumor Necrosis Factor Superfamily in Innate Immunity and Inflammation
Šedý, J., Bekiaris, V., & Ware, C. F. (2015) · Cold Spring Harbor Perspectives in Biology · doi:10.1101/cshperspect.a016279 · Cited by 109
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Metadata
- Authors
- Cheung, T. C., Humphreys, I. R., Potter, K. G., Norris, P. S., Shumway, H. M., Tran, B. R., Patterson, G., Jean-Jacques, R., Yoon, M., Spear, P. G., Murphy, K. M., Lurain, N. S., Benedict, C. A., & Ware, C. F.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 2005-08-30
- Volume
- 102
- Issue
- 37
- Pages
- 13218-13223
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W1867724907
- Cited by
- 209
- References
- 2
- FWCI
- 9.82
- Type
- journal article
- Language
- en
- Open access
- green
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- Cheung, T. C., Humphreys, I. R., Potter, K. G., Norris, P. S., Shumway, H. M., Tran, B. R., Patterson, G., Jean-Jacques, R., Yoon, M., Spear, P. G., Murphy, K. M., Lurain, N. S., Benedict, C. A., & Ware, C. F. (2005). Evolutionarily divergent herpesviruses modulate T cell activation by targeting the herpesvirus entry mediator cosignaling pathway. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.0506172102
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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