Evidence map›Paper›PMID 18795974›Full record

ArticleImmunology2009

Anti-inflammatory effects of tumour necrosis factor (TNF)-alpha are mediated via TNF-R2 (p75) in tolerogenic transforming growth factor-beta-treated antigen-presenting cells.

Sharmila Masli, Bruce Turpie

Open access · bronzeAbstract read
In one paragraph

Article in Immunology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

33 citing papers in PubMed, 64 citations in OpenAlex.

  1. Trial
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  5. Biology · 2024
    Article
  6. Article
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  8. Systemic Cytokines in Retinopathy of Prematurity.Journal of personalized medicine · 2023
    Review
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  10. Article
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  13. Observational
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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

2 authors at 2 institutions in 1 country.

Sharmila MasliDepartment of Ophthalmology, Harvard Medical School, Boston, MA, USA. sharmila.masli@schepens.harvard.edu
Bruce Turpie
Harvard University · USSmith-Kettlewell Eye Research Institute · US

Funding

Molecular Mechanisms Underlying Immune Regulation of Ocular InflammationR01EY015472 · NEI · SCHEPENS EYE RESEARCH INSTITUTE · PI MASLI, SHARMILA · 2004 to 2013
$4.3M
NEI NIH HHS EY015472NEI NIH HHS R01 EY015472
6 · The paper itself

Abstract

Exposure of macrophages to transforming growth factor (TGF)-beta is known to alter their functional phenotype such that antigen presentation by these cells leads to tolerance rather than an inflammatory immune response. Typically, eye-derived antigen-presenting cells (APCs) exposed to TGF-beta in the local environment are known to induce a form of peripheral tolerance and protect the eye from inflammatory immune effector-mediated damage. In response to TGF-beta, APCs increase their expression of tumour necrosis factor (TNF)-alpha and TNF receptor 2 (TNF-R2). Although TNF-alpha has been implicated in tolerance and the associated regulation of the inflammatory immune response, its source and the receptors involved remain unclear. In this report we determined the contribution of TNF-alpha and TNF-R2 expressed by TGF-beta-treated APCs to their anti-inflammatory tolerogenic effect. Our results indicate that APC-derived TNF-alpha is essential for the ability of APCs to regulate the immune response and their IL-12 secretion. Moreover, in the absence of TNF-R2, APCs exposed to TGF-beta failed to induce tolerance or regulatory cells known to participate in this tolerance. Also, blocking of TNF-R1 signalling enhanced the ability of the APCs to secrete increased TGF-beta in response to TGF-beta exposure. Together our results support an anti-inflammatory role of TNF-alpha in regulation of an immune response by TGF-beta-treated APCs and suggest that TNF-R2 contributes significantly to this role.

Indexed as

AnimalsAntigen-Presenting CellsAnti-Inflammatory AgentsCells, CulturedCoculture TechniquesImmune ToleranceImmunophenotypingInterleukin-12Lymphocyte ActivationMiceMice, Inbred C57BLReceptors, Tumor Necrosis Factor, Type IITransforming Growth Factor betaTumor Necrosis Factor-alphaAnti-Inflammatory AgentsInterleukin-12Receptors, Tumor Necrosis Factor, Type IITransforming Growth Factor betaTumor Necrosis Factor-alpha

Identifiers

PMID18795974
PMCPMC2678182
OpenAlexW1600798832

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.