Evidence map›Paper›PMID 18981153›Full record

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

A new mechanism for inhalational priming: IL-4 bypasses innate immune signals.

Anna M Dittrich, Hui-Chen Chen, Lan Xu, Patricia Ranney, Sean Connolly, Timur O Yarovinsky, H Kim Bottomly

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 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

17 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Context matters: TThe Journal of allergy and clinical immunology · 2018
    Article
  5. Review
  6. Article
  7. B Cell-ExtrinsicJournal of immunology (Baltimore, Md. : 1950) · 2017
    Article
  8. Article
  9. Article
  10. Recombinant house dust mite allergens.Methods (San Diego, Calif.) · 2014
    Article
  11. Article
  12. Article
  13. T(H)17 cells mediate pulmonary collateral priming.The Journal of allergy and clinical immunology · 2011
    Article
  14. Facultative role for T cells in extrafollicular Toll-like receptor-dependent autoreactive B-cell responses in vivo.Proceedings of the National Academy of Sciences of the United States of America · 2011
    Article
  15. Article
  16. Importance of cytokines in murine allergic airway disease and human asthma.Journal of immunology (Baltimore, Md. : 1950) · 2010
    Review
  17. 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

7 authors at 1 institution in 1 country.

Anna M DittrichDepartment for Immunobiology, Yale School of Medicine, New Haven, CT 06520, USA. dittrich.anna-maria@mh-hannover.de
Hui-Chen Chen
Lan Xu
Patricia Ranney
Sean Connolly
Timur O Yarovinsky
H Kim Bottomly
Yale University · US

Funding

IMMUNOPATHOGENESIS OF AIRWAY INFLAMMATIONR01HL054450 · NHLBI · YALE UNIVERSITY · PI HERRICK, CHRISTINA A · 1995 to 2007
$3.4M
NHLBI NIH HHS R01 HL054450NHLBI NIH HHS R01 HL54450-09
6 · The paper itself

Abstract

Signaling via innate immune mechanisms is considered pivotal for T cell-mediated responses to inhaled Ags. Furthermore, Th2 cells specific for one inhaled Ag can facilitate priming of naive T cells to unrelated new inhaled Ags, a process we call "Th2 collateral priming". Interestingly, our previous studies showed that collateral priming is independent of signals via the innate immune system but depends on IL-4 secretion by CD4(+) T cells. We thus hypothesized that IL-4 can bypass the need for signals via the innate immune system, considered essential for pulmonary priming. Indeed, we were able to show that IL-4 bypasses the requirement for TLR4- and MyD88-mediated signaling for responses to new allergens. Furthermore, we characterized the mechanisms by which IL-4 primes for new inhaled allergens: "IL-4-dependent pulmonary priming" relies on IL-4 receptor expression on hematopoietic cells and structural cells. Transfer experiments indicate that within the hematopoietic compartment both T cells and dendritic cells need to express the IL-4 receptor. Finally, we were able to show that IL-4 induces recruitment and maturation of myeloid dendritic cells in vivo and increases T cell recruitment to the draining lymph nodes. Our findings bring new mechanistic knowledge to the phenomenon of polysensitization and primary sensitization in asthma.

Indexed as

Administration, InhalationAdoptive TransferAnimalsAntigen PresentationCD4-Positive T-LymphocytesChemotaxis, LeukocyteDendritic CellsFlow CytometryInterleukin-4Lymphocyte ActivationMiceMice, Inbred BALB CMice, KnockoutOvalbuminPneumoniaInterleukin-4Ovalbumin

Identifiers

PMID18981153
PMCPMC2692059
OpenAlexW2118226418

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.