Evidence map›Paper›PMID 14678266›Full record

ArticleClinical and experimental immunology2004

Molecular mechanisms of interleukin-10-mediated inhibition of NF-kappaB activity: a role for p50.

F Driessler, K Venstrom, R Sabat, K Asadullah, A J Schottelius

Open access · greenAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 124 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
124citing papers in PubMed, 2 pooled it
3.9field-weighted citation impact, top 6% 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

124 citing papers in PubMed, 2 syntheses or guidelines pooled it, 269 citations in OpenAlex.

  1. Pooled it
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  10. Foods (Basel, Switzerland) · 2026
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  18. The Importance of Phosphoinositide 3-Kinase in Neuroinflammation.International journal of molecular sciences · 2024
    Review
  19. Article
  20. Article

64 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

5 authors.

F DriesslerResearch Business Area Dermatology, Research Laboratories of Schering AG, Berlin, Germany.
K Venstrom
R Sabat
K Asadullah
A J Schottelius

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nuclear factor kappa B (NF-kappaB) is a transcription factor pivotal for the development of inflammation. A dysregulation of NF-kappaB has been shown to play an important role in many chronic inflammatory diseases including rheumatoid arthritis, inflammatory bowel disease and psoriasis. Although classical NF-kappaB, a heterodimer composed of the p50 and p65 subunits, has been well studied, little is known about gene regulation by other hetero- and homodimeric forms of NF-kappaB. While p65 possesses a transactivation domain, p50 does not. Indeed, p50/p50 homodimers have been shown to inhibit transcriptional activity. We have recently shown that Interleukin-10 exerts its anti-inflammatory activity in part through the inhibition of NF-kappaB by blocking IkappaB kinase activity and by inhibiting NF-kappaB already found in the nucleus. Since the inhibition of nuclear NF-kappaB could not be explained by an increase of nuclear IkappaB, we sought to further investigate the mechanisms involved in the inhibition of NF-kappaB by IL-10. We show here that IL-10 selectively induced nuclear translocation and DNA-binding of p50/p50 homodimers in human monocytic cells. TNF-alpha treatment led to a strong translocation of p65 and p50, whereas pretreatment with IL-10 followed by TNF-alpha blocked p65 translocation but did not alter the strong translocation of p50. Furthermore, macrophages of p105/p50-deficient mice exhibited a significantly decreased constitutive production of MIP-2alpha and IL-6 in comparison to wild type controls. Surprisingly, IL-10 inhibited high constitutive levels of these cytokines in wt macrophages but not in p105/p50 deficient cells. Our findings suggest that the selective induction of nuclear translocation and DNA-binding of the repressive p50/p50 homodimer is an important anti-inflammatory mechanism utilized by IL-10 to repress inflammatory gene transcription.

Indexed as

AnimalsCells, CulturedHumansInterleukin-10LipopolysaccharidesMacrophages, PeritonealMiceMice, Inbred StrainsNF-kappa BNF-kappa B p50 SubunitProtein PrecursorsRecombinant ProteinsTranscription Factor RelATranslocation, GeneticTumor Necrosis Factor-alphaInterleukin-10LipopolysaccharidesNF-kappa BNF-kappa B p50 SubunitProtein PrecursorsRecombinant ProteinsTranscription Factor RelATumor Necrosis Factor-alpha

Identifiers

PMID14678266
PMCPMC1808913
OpenAlexW1999881028

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.