Evidence map›Paper›PMID 11342593›Full record

ArticleThe Journal of experimental medicine2001

Signal transducer and activator of transcription 6 controls chemokine production and T helper cell type 2 cell trafficking in allergic pulmonary inflammation.

A Mathew, J A MacLean, E DeHaan, A M Tager, F H Green, A D Luster

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 1 pooled it
8.3field-weighted citation impact, top 2% 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

52 citing papers in PubMed, 1 synthesis or guideline pooled it, 180 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. The Impact of the CBMolecules (Basel, Switzerland) · 2024
    Review
  4. Article
  5. Exercise and Asthma.Advances in experimental medicine and biology · 2020
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. A hypothesis-effect of T cell epitope fusion peptide specific immunotherapy on signal transduction.International journal of clinical and experimental medicine · 2015
    Article
  14. Key mediators in the immunopathogenesis of allergic asthma.International immunopharmacology · 2014
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  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 3 institutions in 2 countries.

A MathewCenter for Immunology and Inflammatory Diseases, Division of Rheumatology, Allergy, and Immunology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114, USA.
J A MacLean
E DeHaan
A M Tager
F H Green
A D Luster
Harvard University · USMassachusetts General Hospital · USUniversity of Calgary · CA

Funding

Lung-Resident Memory Th2 cells in Asthma - New Therapeutic TargetsR01AI040618 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI LUSTER, ANDREW D · 1997 to 2022
$5.6M
ROLE OF TH2 CELLS IN EOTAXIN REGULATIONF32HL010375 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI MATHEW, ANUJA · 2000 to 2002
$119k
NHLBI NIH HHS F32 HL010375NHLBI NIH HHS F32-HL10375-01NIAID NIH HHS R01-AI40618
6 · The paper itself

Abstract

Antigen-specific CD4 T helper type 2 (Th2) cells play a pivotal role in the induction of allergic asthma, but the mechanisms regulating their recruitment into the airways are unknown. Signal transducer and activator of transcription factor (Stat)6 is a transcription factor essential for Th2 cell differentiation. Here we show that Stat6 also controls Th2 cell recruitment and effector function in allergic inflammation in vivo. To isolate the role of Stat6 in regulating Th2 cell trafficking and effector function from its role in Th2 cell differentiation, we used a murine model of asthma in which in vitro-differentiated Stat6(+/+) antigen-specific Th2 cells were adoptively transferred into naive Stat6(-/-) and Stat6(+/+) mice followed by aerosol antigen challenge. We found that all of the features of asthma, including Th2 cell accumulation, Th2 and eosinophil-active chemokine production, and airway eosinophilia, mucus production, and hyperresponsiveness seen in Stat6(+/+) mice, were dramatically absent in Stat6(-/)- mice that received Stat6(+/)+ antigen-specific Th2 cells. Our findings establish Stat6 as essential for Th2 cell trafficking and effector function and suggest that interruption of Stat6 signaling in resident cells of the lung is a novel approach to asthma therapy.

Indexed as

Transcriptional ActivationAnimalsAntigensBronchial HyperreactivityBronchoalveolar Lavage FluidChemokinesCytokinesEosinophilsGene Expression ProfilingGoblet CellsLungMiceMice, Inbred BALB CMice, KnockoutMice, TransgenicMucusAntigensChemokinesCytokinesOvalbuminStat6 protein, mouseSTAT6 Transcription FactorTrans-Activators

Identifiers

PMID11342593
PMCPMC2193434
OpenAlexW2022689552

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.