Evidence map›Paper›PMID 19050285›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2008

Antagonism of airway tolerance by endotoxin/lipopolysaccharide through promoting OX40L and suppressing antigen-specific Foxp3+ T regulatory cells.

Wei Duan, Takanori So, Michael Croft

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

47 citing papers in PubMed, 74 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Article
  4. Article
  5. NOD2-NLRP3 Axis and Asthma.Journal of asthma and allergy · 2025
    Review
  6. Article
  7. Combination blockade of OX40L and CD30L inhibits allergen-driven memory TThe Journal of allergy and clinical immunology · 2021
    Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Mechanisms of Oral Tolerance.Clinical reviews in allergy & immunology · 2018
    Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  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

3 authors at 1 institution in 1 country.

Wei DuanDivision of Molecular Immunology, La Jolla Institute for Allergy and Immunology, La Jolla, CA 92037, USA.
Takanori So
Michael Croft
La Jolla Institute for Immunology · US

Funding

TRM and airway inflammation and remodelingU19AI070535 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BROIDE, DAVID H · 2006 to 2025
$34.2M
Regulation of T Cell Tolerance by OX40R01CA091837 · NCI · LA JOLLA INSTITUTE FOR IMMUNOLOGY · PI CROFT, MICHAEL · 2002 to 2012
$2.5M
NCI NIH HHS CA91837NCI NIH HHS R01 CA091837NIAID NIH HHS AI070535NIAID NIH HHS U19 AI070535
6 · The paper itself

Abstract

Respiratory exposure to allergens can lead to airway tolerance. Factors that antagonize tolerance mechanisms in the lung might result in susceptibility to diseases such as asthma. We show that inhalation of endotoxin/LPS with Ag prevented airway tolerance and abolished protection from T cell-driven asthmatic lung inflammation. Under conditions leading to tolerance, adaptive Ag-specific CD4(+)Foxp3(+) T regulatory cells (Treg) were generated following exposure to intranasal Ag and outnumbered IL-4- and IFN-gamma-producing CD4 T cells by 100:1 or greater. Inhaled LPS altered the ratio of Treg to IL-4(+) or IFN-gamma(+) T cells by concomitantly suppressing Treg generation and promoting effector T cell generation. LPS induced OX40L expression on dendritic cells and B cells that resulted in a synergistic activity between TLR4 and OX40 signals, leading to production of IL-4, IFN-gamma, and IL-6, which blocked Treg development. Furthermore, inhibiting OX40/OX40L interactions prevented LPS from suppressing tolerance, and resulted in the generation of greater numbers of adaptive Treg. Thus, cooperation between TLR4 and OX40 controls susceptibility to developing airway disease via modulating the balance between adaptive Treg and IL-4(+) or IFN-gamma(+) T cells. Targeting OX40L then has the potential to improve the efficacy of Ag immunotherapy to promote tolerance.

Indexed as

Immune ToleranceAdministration, IntranasalAllergensAnimalsCD4-Positive T-LymphocytesCells, CulturedDesensitization, ImmunologicEpitopes, T-LymphocyteForkhead Transcription FactorsInflammation MediatorsLipopolysaccharidesMembrane GlycoproteinsMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicAllergensEpitopes, T-LymphocyteForkhead Transcription FactorsFoxp3 protein, mouseInflammation MediatorsLipopolysaccharidesMembrane GlycoproteinsOvalbuminOX40 LigandReceptors, OX40Tnfrsf4 protein, mouseTnfsf4 protein, mouseTumor Necrosis Factor InhibitorsTumor Necrosis Factors

Identifiers

PMID19050285
PMCPMC2596654
OpenAlexW2169706949

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.