Evidence map›Paper›PMID 25905673›Full record

ArticleeLife2015

Stimulus-selective crosstalk via the NF-κB signaling system reinforces innate immune response to alleviate gut infection.

Balaji Banoth, Budhaditya Chatterjee, Bharath Vijayaragavan, M V R Prasad, Payel Roy, Soumen Basak

Open access · goldAbstract read
In one paragraph

Article in eLife, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

34 citing papers in PubMed, 59 citations in OpenAlex.

  1. Review
  2. Toxicology reports · 2025
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  7. Review
  8. NFκB signaling in T cell memory.Frontiers in immunology · 2023
    Review
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  12. Review
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  14. Review
  15. Molecular mechanisms of lidocaine.Annals of medicine and surgery (2012) · 2021
    Review
  16. An epithelialProceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  17. Article
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  20. Article
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

6 authors at 1 institution in 1 country.

Balaji BanothSystems Immunology Laboratory, National Institute of Immunology, New Delhi, India.
Budhaditya ChatterjeeSystems Immunology Laboratory, National Institute of Immunology, New Delhi, India.
Bharath VijayaragavanSystems Immunology Laboratory, National Institute of Immunology, New Delhi, India.
M V R PrasadSystems Immunology Laboratory, National Institute of Immunology, New Delhi, India.
Payel RoySystems Immunology Laboratory, National Institute of Immunology, New Delhi, India.
Soumen BasakSystems Immunology Laboratory, National Institute of Immunology, New Delhi, India.
National Institute of Immunology · IN

Funding

Wellcome Trust
6 · The paper itself

Abstract

Tissue microenvironment functions as an important determinant of the inflammatory response elicited by the resident cells. Yet, the underlying molecular mechanisms remain obscure. Our systems-level analyses identified a duration code that instructs stimulus specific crosstalk between TLR4-activated canonical NF-κB pathway and lymphotoxin-β receptor (LTβR) induced non-canonical NF-κB signaling. Indeed, LTβR costimulation synergistically enhanced the late RelA/NF-κB response to TLR4 prolonging NF-κB target gene-expressions. Concomitant LTβR signal targeted TLR4-induced newly synthesized p100, encoded by Nfkb2, for processing into p52 that not only neutralized p100 mediated inhibitions, but potently generated RelA:p52/NF-κB activity in a positive feedback loop. Finally, Nfkb2 connected lymphotoxin signal within the intestinal niche in reinforcing epithelial innate inflammatory RelA/NF-κB response to Citrobacter rodentium infection, while Nfkb2(-/-) mice succumbed to gut infections owing to stromal defects. In sum, our results suggest that signal integration via the pleiotropic NF-κB system enables tissue microenvironment derived cues in calibrating physiological responses.

Indexed as

AnimalsCitrobacter rodentiumEnterobacteriaceae InfectionsGene Expression RegulationImmunity, InnateInflammationIntestinal MucosaLymphotoxin beta ReceptorMiceMice, Inbred C57BLMice, KnockoutNF-kappa BNF-kappa B p52 SubunitSignal TransductionTranscription Factor RelALymphotoxin beta ReceptorNF-kappa BNF-kappa B p52 SubunitNfkb2 protein, mouseRela protein, mouseTranscription Factor RelACitrobacter rodentiumcomputational biologyimmunologyinflammationinnate immunitylymphotoxinmousepositive feedbackRelA:p52/NF-kappaBsystems biology

Identifiers

PMID25905673
PMCPMC4432492
OpenAlexW2098869905

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.