B and T lymphocyte attenuator regulates T cell activation through interaction with herpesvirus entry mediator

By J. Šedý, Maya Gavrieli, Karen G. Potter, Michelle A. Hurchla, R. C. Lindsley, K. Hildner, S. Scheu, K. Pfeffer, C. Ware, T. Murphy and 1 more. Nature Immunology, 2005

644 citations recorded by the source corpus.

Subfields: Epidemiology, Immunology

View Paper: https://www.semanticscholar.org/paper/535be85cc67260931a82003c29bc2662c9542976

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In Epidemiology

1. W. Zou

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Citations in the corpus

• The blockade of immune checkpoints in cancer immunotherapy (2012, background): “Subsequently, herpesvirus entry mediator (HVEM; also known as TNFRSF14) — which is expressed on certain tumour cell types (for example, melanoma) as well as on tumour-associated endothelial cells — was shown to be the BTLA ligan”
• Inhibitory B7-family molecules in the tumour microenvironment (2008, background): “32 ), but recent studies show that this is not the case and that herpes virus entry mediator is the ligand for BTL”
• Mechanisms of immune evasion by tumors. (2006, background): “While CTLA‐4 and PD1 bind to B7 family members, the ligand for BTLA has been identified as HVEM (herpesvirus entry mediator) (Sedy et al., 2005), which is a member of the TNFR superfamily (Croft et al., 2005).”
• Novel immune checkpoint targets: moving beyond PD-1 and CTLA-4 (2019, methodology): “Herpesvirus entry mediator (HVEM), a member of the tumor necrosis factor receptor superfamily (TNFRSF), was identified as the unique BTLA ligand in 2005 [131].”