Evidence map›Paper›PMID 22593615›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2012

RGS16 attenuates pulmonary Th2/Th17 inflammatory responses.

Sucharita P Shankar, Mark S Wilson, Jeffrey A DiVietro, Margaret M Mentink-Kane, Zhihui Xie, Thomas A Wynn, Kirk M Druey

Open access · greenAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

24 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
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  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Normal Thymocyte Egress, T Cell Trafficking, and CD4Journal of immunology (Baltimore, Md. : 1950) · 2017
    Article
  14. Article
  15. Review
  16. RGS proteins as targets in the treatment of intestinal inflammation and visceral pain: New insights and future perspectives.BioEssays : news and reviews in molecular, cellular and developmental biology · 2016
    Review
  17. Review
  18. Article
  19. Article
  20. RGS3 controls T lymphocyte migration in a model of Th2-mediated airway inflammation.American journal of physiology. Lung cellular and molecular physiology · 2013
    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 2 institutions in 1 country.

Sucharita P ShankarMolecular Signal Transduction Section, Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Mark S Wilson
Jeffrey A DiVietro
Margaret M Mentink-Kane
Zhihui Xie
Thomas A Wynn
Kirk M Druey
National Institute of Allergy and Infectious Diseases · USNational Institutes of Health · US

Funding

Approaches To Immunological Intervention In SchistosomiasisZIAAI000829 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI WYNN, THOMAS · 2009 to 2018
$9.9M
Heterotrimeric G Protein Signaling In Allergic InflammationZIAAI000746 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI DRUEY, KIRK M · 2009 to 2025
$4.6M
HETEROTRIMERIC G PROTEIN SIGNALING IN ALLERGIC INFLAMMATIONZ01AI000746 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI DRUEY, KIRK M · 1998 to 2008
$1.1M
Intramural NIH HHS Z01 AI000746Intramural NIH HHS ZIA AI000746Medical Research Council MC_UP_A253_1028
6 · The paper itself

Abstract

The regulators of G protein signaling (RGS) protein superfamily negatively controls G protein-coupled receptor signal transduction pathways. RGS16 is enriched in activated/effector T lymphocytes. In this paper, we show that RGS16 constrains pulmonary inflammation by regulating chemokine-induced T cell trafficking in response to challenge with Schistosoma mansoni. Naive Rgs16(-/-) mice were "primed" for inflammation by accumulation of CCR10(+) T cells in the lung. Upon pathogen exposure, these mice developed more robust granulomatous lung fibrosis than wild-type counterparts. Distinct Th2 or putative Th17 subsets expressing CCR4 or CCR10 accumulated more rapidly in Rgs16(-/-) lungs following challenge and produced proinflammatory cytokines IL-13 and IL-17B. CCR4(+)Rgs16(-/-) Th2 cells migrated excessively to CCL17 and localized aberrantly in challenged lungs. T lymphocytes were partially excluded from lung granulomas in Rgs16(-/-) mice, instead forming peribronchial/perivascular aggregates. Thus, RGS16-mediated confinement of T cells to Schistosome granulomas mitigates widespread cytokine-mediated pulmonary inflammation.

Indexed as

AnimalsChemotaxis, LeukocyteCytokinesFlow CytometryImmunohistochemistryMiceMice, Inbred C57BLMice, KnockoutPneumoniaReal-Time Polymerase Chain ReactionRGS ProteinsSchistosomiasis mansoniTh17 CellsTh2 CellsCytokinesRGS16 proteinRGS Proteins

Identifiers

PMID22593615
PMCPMC3522182
OpenAlexW2126914896

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.