Evidence map›Paper›PMID 22438258›Full record

ArticleBlood2012

The tyrosine phosphatase SHP-1 dampens murine Th17 development.

Ileana S Mauldin, Kenneth S Tung, Ulrike M Lorenz

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

18 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Observational
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Tumor necrosis factor superfamily in innate immunity and inflammation.Cold Spring Harbor perspectives in biology · 2014
    Review
  15. Article
  16. Article
  17. Article
  18. 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 2 institutions in 1 country.

Ileana S MauldinBeirne Carter Center for Immunology Research and Department of Microbiology, Immunology, and Cancer Biology, University of Virginia, Charlottesville, VA 22908, USA.
Kenneth S Tung
Ulrike M Lorenz
Carter Center · USUniversity of Virginia · US

Funding

ZONA PELLUCIDA--IMMUNOPATHOLOGIC STUDYR01AI041236 · NIAID · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI TUNG, KENNETH S.K. · 1996 to 2017
$5.2M
Global Biothreats Training ProgramT32AI055432 · NIAID · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI CRISS, ALISON K, PETRI, WILLIAM A · 2003 to 2022
$4.0M
Antibody induced T cell-mediated neonatal autoimmunity.R01AI051420 · NIAID · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI TUNG, KENNETH S.K. · 2003 to 2012
$3.4M
Role of SHP-1 in T cell activation and developmentR01AI048672 · NIAID · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI LORENZ, ULRIKE · 2001 to 2009
$3.3M
Antibody-induced T cell-mediated neonatal autoimmunityR21AI051420 · NIAID · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI TUNG, KENNETH S.K. · 2002 to 2002
$332k
NIAID NIH HHS AI 41236NIAID NIH HHS AI 51420NIAID NIH HHS R01 AI041236NIAID NIH HHS R01 AI048672NIAID NIH HHS R01 AI051420NIAID NIH HHS R01 AI48672NIAID NIH HHS R21 AI051420NIAID NIH HHS T32 AI055432
6 · The paper itself

Abstract

Th17 cells represent a subset of CD4+ T helper cells that secrete the proinflammatory cytokine IL-17. Th17 cells have been ascribed both a beneficial role in promoting clearance of pathogenic fungi and bacteria, and a pathogenic role in autoimmune diseases. Here we identify the tyrosine phosphatase SHP-1 as a critical regulator of Th17 development, using 3 complementary approaches. Impaired SHP-1 activity through genetic deletion of SHP-1, transgenic expression of an inducible dominant negative SHP-1, or pharmacologic inhibition of SHP-1 strongly promotes the development of Th17. Ex vivo Th17 skewing assays demonstrate that genetic or pharmacologic disruption of SHP-1 activity in T cells results in a hyper-response to stimulation via IL-6 and IL-21, 2 cytokines that promote Th17 development. Mechanistically, we find that SHP-1 decreases the overall cytokine-induced phosphorylation of STAT3 in primary CD4+ T cells. These data identify SHP-1 as a key modifier of IL-6-and IL-21-driven Th17 development via regulation of STAT3 signaling and suggest SHP-1 as a potential new therapeutic target for manipulating Th17 differentiation in vivo.

Indexed as

AnimalsCell DifferentiationCells, CulturedColitisDown-RegulationInterleukin-21Interleukin-6InterleukinsIntestinal MucosaIntestinesMiceMice, Inbred BALB CMice, Inbred C57BLMice, TransgenicProtein Tyrosine Phosphatase, Non-Receptor Type 6Protein Tyrosine PhosphatasesInterleukin-21Interleukin-6InterleukinsProtein Tyrosine Phosphatase, Non-Receptor Type 6Protein Tyrosine PhosphatasesPtpn6 protein, mouse

Identifiers

PMID22438258
PMCPMC3362360
OpenAlexW1985889257

What OpenQuestion holds

Textmetadata
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.