Evidence map›Paper›PMID 22017438›Full record

ReviewImmunological reviews2011

The signaling networks of the herpesvirus entry mediator (TNFRSF14) in immune regulation.

Marcos W Steinberg, Timothy C Cheung, Carl F Ware

Open access · greenAbstract readReview
In one paragraph

Review in Immunological reviews, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 146 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
146citing papers in PubMed, 1 pooled it
6.8field-weighted citation impact, top 3% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

146 citing papers in PubMed, 1 synthesis or guideline pooled it, 238 citations in OpenAlex.

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86 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Marcos W SteinbergLaboratory of Molecular Immunology, Center for Infectious and Inflammatory Diseases, Sanford|Burnham Medical Research Institute, La Jolla, CA 92037, USA.
Timothy C Cheung
Carl F Ware
Sanford Burnham Prebys Medical Discovery Institute · US

Funding

Anti-herpesvirus Signaling by LTalphabeta/LIGHT CytokinesR01AI048073 · NIAID · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI WARE, CARL F · 2001 to 2016
$7.0M
HVEM-BTLA system in InflammationR01AI067890 · NIAID · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI WARE, CARL F · 2007 to 2016
$4.3M
Lymphotoxin alpha Beta and LIGHT cytokine systemsR37AI033068 · NIAID · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI WARE, CARL F · 2003 to 2012
$4.2M
Human Lymphoid Tissue InducersR21AI088445 · NIAID · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI WARE, CARL F · 2010 to 2011
$522k
Self Complementary Recombinant AAV VectorsR01AI048074 · NIAID · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI MCCARTY, DOUGLAS M · 2003 to 2005
$431k
NIAID NIH HHS AI048074NIAID NIH HHS AI067890NIAID NIH HHS R01 AI048073NIAID NIH HHS R01 AI048074NIAID NIH HHS R01 AI067890NIAID NIH HHS R21 AI088445NIAID NIH HHS R37 AI033068NIAID NIH HHS R37AI33068
6 · The paper itself

Abstract

The tumor necrosis factor (TNF) receptor superfamily member herpesvirus entry mediator (HVEM) (TNFRSF14) regulates T-cell immune responses by activating both inflammatory and inhibitory signaling pathways. HVEM acts as both a receptor for the canonical TNF-related ligands, LIGHT [lymphotoxin-like, exhibits inducible expression, and competes with herpes simplex virus glycoprotein D for HVEM, a receptor expressed on T lymphocytes] and lymphotoxin-α, and as a ligand for the immunoglobulin superfamily proteins BTLA (B and T lymphocyte attenuator) and CD160, a feature distinguishing HVEM from other immune regulatory molecules. The ability of HVEM to interact with multiple ligands in distinct configurations creates a functionally diverse set of intrinsic and bidirectional signaling pathways that control both inflammatory and inhibitory responses. The HVEM system is integrated into the larger LTβR and TNFR network through extensive shared ligand and receptor usage. Experimental mouse models and human diseases indicate that dysregulation of HVEM network may contribute to autoimmune pathogenesis, making it an attractive target for drug intervention.

Indexed as

Immunity, InnateReceptors, Tumor Necrosis Factor, Member 14AnimalsAntigens, CDAutoimmunityGene ExpressionGPI-Linked ProteinsHerpes SimplexHerpesvirus 1, HumanHumansLymphocyte ActivationLymphotoxin-alphaLymphotoxin beta ReceptorMiceMice, KnockoutProtein BindingAntigens, CDCD160 protein, humanglycoprotein D, Human herpesvirus 1GPI-Linked ProteinsLymphotoxin-alphaLymphotoxin beta ReceptorReceptors, ImmunologicReceptors, Tumor Necrosis Factor, Member 14TNFRSF14 protein, humanTumor Necrosis Factor-alphaTumor Necrosis Factor Ligand Superfamily Member 14Viral Envelope Proteins

Identifiers

PMID22017438
PMCPMC3381650
OpenAlexW1480075263

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.