Evidence map›Paper›PMID 18613837›Full record

ReviewImmunological reviews2008

Targeting lymphocyte activation through the lymphotoxin and LIGHT pathways.

Carl F Ware

Open access · greenAbstract readReview
In one paragraph

Review in Immunological reviews, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

69 citing papers in PubMed, 116 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Aberrant Expression ofCancers · 2025
    Article
  6. Review
  7. Recognition ofBiology · 2024
    Article
  8. Review
  9. Article
  10. Review
  11. LIGHT Amplification by NF-Mediators of inflammation · 2023
    Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. Review

9 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

1 author at 1 institution in 1 country.

Carl F WareDivision of Molecular Immunology, La Jolla Institute for Allergy and Immunology, La Jolla, CA 92037, USA. cware@liai.org
La Jolla Institute for Immunology · 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
NIAID NIH HHS AI048073NIAID NIH HHS AI067890NIAID NIH HHS R01 AI048073NIAID NIH HHS R01 AI067890NIAID NIH HHS R37 AI033068NIAID NIH HHS R37AI33068
6 · The paper itself

Abstract

summaryCytokines mediate key communication pathways essential for regulation of immune responses. Full activation of antigen-responding lymphocytes requires cooperating signals from the tumor necrosis factor (TNF)-related cytokines and their specific receptors. LIGHT, a lymphotoxin-beta (LTbeta)-related TNF family member, modulates T-cell activation through two receptors, the herpesvirus entry mediator (HVEM) and indirectly through the LT-beta receptor. An unexpected finding revealed a non-canonical binding site on HVEM for the immunoglobulin superfamily member, B and T lymphocyte attenuator (BTLA), and an inhibitory signaling protein suppressing T-cell activation. Thus, HVEM can act as a molecular switch between proinflammatory and inhibitory signaling. The non-canonical HVEM-BTLA pathway also acts to counter LTbetaR signaling that promotes the proliferation of antigen-presenting dendritic cells (DCs) within lymphoid tissue microenvironments. These results indicate LTbeta receptor and HVEM-BTLA pathways form an integrated signaling circuit. Targeting these cytokine pathways with specific antagonists (antibody or decoy receptor) can alter lymphocyte differentiation and activation. Alternately, agonists directed at their cell surface receptors can restore homeostasis and potentially reset immune and inflammatory processes, which may be useful in treating autoimmune and infectious diseases and cancer.

Indexed as

AnimalsAutoimmune DiseasesDendritic CellsFeedback, PhysiologicalHumansLymphocyte ActivationLymphotoxin alpha1, beta2 HeterotrimerLymphotoxin beta ReceptorMiceReceptor Cross-TalkReceptors, ImmunologicReceptors, Tumor Necrosis Factor, Member 14Signal TransductionT-LymphocytesTumor Necrosis Factor Ligand Superfamily Member 14BTLA protein, humanLymphotoxin alpha1, beta2 HeterotrimerLymphotoxin beta ReceptorReceptors, ImmunologicReceptors, Tumor Necrosis Factor, Member 14Tumor Necrosis Factor Ligand Superfamily Member 14

Identifiers

PMID18613837
PMCPMC2613484
OpenAlexW2162977630

What OpenQuestion holds

Textmetadata
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.