Evidence map›Paper›PMID 18802110›Full record

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

STAT4 isoforms differentially regulate Th1 cytokine production and the severity of inflammatory bowel disease.

John T O'Malley, Rajaraman D Eri, Gretta L Stritesky, Anubhav N Mathur, Hua-Chen Chang, Harm Hogenesch, Mythily Srinivasan, Mark H Kaplan

Open access · bronzeAbstract readComparative Study
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 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing 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

22 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Activation pathways that drive CD4Immunological reviews · 2022
    Review
  5. Review
  6. STAT4: an immunoregulator contributing to diverse human diseases.International journal of biological sciences · 2020
    Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. GM-CSF as a therapeutic target in autoimmune diseases.Inflammation and regeneration · 2016
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  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

8 authors at 3 institutions in 1 country.

John T O'MalleyDepartment of Pediatrics, HB Wells Center for Pediatric Research and Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Rajaraman D Eri
Gretta L Stritesky
Anubhav N Mathur
Hua-Chen Chang
Harm Hogenesch
Mythily Srinivasan
Mark H Kaplan
Indiana University – Purdue University Indianapolis · USIndiana University School of MedicinePurdue University West Lafayette · US

Funding

The role of PU.1 in T helper cell heterogeneityR01AI057459 · NIAID · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI KAPLAN, MARK H · 2005 to 2025
$8.2M
Immunology and Infectious Diseases Training ProgramT32AI060519 · NIAID · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI MARK H KAPLAN · 2004 to 2026
$6.0M
STAT4 IMMUNOLOGYR01AI045515 · NIAID · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI KAPLAN, MARK H · 1999 to 2014
$4.3M
Stat4 ImmunobiologyR56AI045515 · NIAID · INDIANA UNIVERSITY INDIANAPOLIS · PI KAPLAN, MARK H · 2009 to 2009
$385k
NIAID NIH HHS AI45515NIAID NIH HHS AI57459NIAID NIH HHS R01 AI045515NIAID NIH HHS R01 AI057459NIAID NIH HHS R56 AI045515NIAID NIH HHS T32 AI060519NIAID NIH HHS T32AI060519
6 · The paper itself

Abstract

STAT4, a critical regulator of inflammation in vivo, can be expressed as two alternative splice forms, a full-length STAT4alpha, and a STAT4beta isoform lacking a C-terminal transactivation domain. Each isoform is sufficient to program Th1 development through both common and distinct subsets of target genes. However, the ability of these isoforms to mediate inflammation in vivo has not been examined. Using a model of colitis that develops following transfer of CD4(+) CD45RB(high) T cells expressing either the STAT4alpha or STAT4beta isoform into SCID mice, we determined that although both isoforms mediate inflammation and weight loss, STAT4beta promotes greater colonic inflammation and tissue destruction. This correlates with STAT4 isoform-dependent expression of TNF-alpha and GM-CSF in vitro and in vivo, but not Th1 expression of IFN-gamma or Th17 expression of IL-17, which were similar in STAT4alpha- and STAT4beta-expressing T cells. Thus, higher expression of a subset of inflammatory cytokines from STAT4beta-expressing T cells correlates with the ability of STAT4beta-expressing T cells to mediate more severe inflammatory disease.

Indexed as

Severity of Illness IndexAnimalsCells, CulturedCytokinesFemaleInflammation MediatorsInflammatory Bowel DiseasesLymphocyte TransfusionMiceMice, Inbred C57BLMice, KnockoutMice, SCIDMice, TransgenicProtein IsoformsProtein Structure, TertiaryReceptors, Antigen, T-CellCytokinesInflammation MediatorsProtein IsoformsReceptors, Antigen, T-CellStat4 protein, mouseSTAT4 Transcription FactorTumor Necrosis Factor-alpha

Identifiers

PMID18802110
PMCPMC2596939
OpenAlexW2127081443

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.