Evidence map›Paper›PMID 11544280›Full record

ArticleThe Journal of clinical investigation2001

Effect of targeted disruption of STAT4 and STAT6 on the induction of experimental autoimmune encephalomyelitis.

T Chitnis, N Najafian, C Benou, A D Salama, M J Grusby, M H Sayegh, S J Khoury

Open access · greenAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
102citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 5% 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

102 citing papers in PubMed, 1 synthesis or guideline pooled it, 212 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. An IL-23-STAT4 pathway is required for the proinflammatory function of classical dendritic cells during CNS inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  5. STAT4 gene polymorphisms in human diseases.Frontiers in immunology · 2024
    Review
  6. The Exposure to Lead (Pb) Exacerbates Immunological Abnormalities in BTBR TInternational journal of molecular sciences · 2023
    Article
  7. Article
  8. STAT6 suppression prevents bleomycin-induced dermal fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023
    Article
  9. Article
  10. Article
  11. Review
  12. Activation pathways that drive CD4Immunological reviews · 2022
    Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Review
  19. Review
  20. Review

42 more citing papers are in PubMed but not listed here.

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.

T ChitnisCenter for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.
N Najafian
C Benou
A D Salama
M J Grusby
M H Sayegh
S J Khoury
Harvard University · USBrigham and Women's Hospital · US

Funding

T Cell Fate as a Determinant of Alloimmune ResponsesP01AI041521 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI STROM, TERRY B. · 1997 to 2011
$15.9M
NIAID NIH HHS P01 AI041521NIAID NIH HHS P01 AI-41521
6 · The paper itself

Abstract

Experimental autoimmune encephalomyelitis (EAE) is mediated by myelin-specific CD4(+) T cells secreting Th1 cytokines, while recovery from disease is associated with expression of Th2 cytokines. Investigations into the role of individual cytokines in disease induction have yielded contradictory results. Here we used animals with targeted deletion of the STAT4 or STAT6 genes to determine the role of these signaling molecules in EAE. The STAT4 pathway controls the differentiation of cells into a Th1 phenotype, while the STAT6 pathway controls the differentiation of cells into a Th2 phenotype. We found that mice deficient in STAT4 are resistant to the induction of EAE, with minimal inflammatory infiltrates in the central nervous system. In contrast, STAT6-deficient mice, which have a predominantly Th1 phenotype, experience a more severe clinical course of EAE as compared with wild-type or STAT4 knockout mice. In addition, adoptive transfer studies confirm the regulatory functions of a Th2 environment in vivo. These novel data indicate that STAT4 and STAT6 genes play a critical role in regulating the autoimmune response in EAE.

Indexed as

Adoptive TransferAnimalsCells, CulturedCentral Nervous SystemCytokinesDNA-Binding ProteinsEncephalomyelitis, Autoimmune, ExperimentalGene TargetingImmunoglobulin GMiceMice, Inbred C57BLMice, KnockoutMyelin-Associated GlycoproteinMyelin-Oligodendrocyte GlycoproteinMyelin ProteinsReceptors, Antigen, T-Cell, alpha-betaCytokinesDNA-Binding ProteinsImmunoglobulin GMog protein, mouseMyelin-Associated GlycoproteinMyelin-Oligodendrocyte GlycoproteinMyelin ProteinsReceptors, Antigen, T-Cell, alpha-betaStat4 protein, mouseSTAT4 Transcription FactorStat6 protein, mouseSTAT6 Transcription FactorTrans-Activators

Identifiers

PMID11544280
PMCPMC209380
OpenAlexW2057658272

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.