Evidence map›Paper›PMID 9032280›Full record

ArticleMolecular and cellular biology1997

Transcription mediated by NFAT is highly inducible in effector CD4+ T helper 2 (Th2) cells but not in Th1 cells.

M Rincón, R A Flavell

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
5.6field-weighted citation impact, top 3% 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

32 citing papers in PubMed, 116 citations in OpenAlex.

  1. How does NFAT3 regulate the occurrence of cardiac hypertrophy?International journal of cardiology. Heart & vasculature · 2023
    Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Transcriptional control of rapid recall by memory CD4 T cells.Journal of immunology (Baltimore, Md. : 1950) · 2011
    Article
  10. Article
  11. Article
  12. Accumulation of NFAT mediates IL-2 expression in memory, but not naïve, CD4+ T cells.Proceedings of the National Academy of Sciences of the United States of America · 2007
    Article
  13. Article
  14. Article
  15. Carcinogenic effect of nickel compounds.Molecular and cellular biochemistry · 2005
    Review
  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

2 authors at 2 institutions in 1 country.

M RincónSection of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06510, USA.
R A Flavell
Howard Hughes Medical Institute · USYale University · US

Funding

NOVEL AUTOIMMUNITY IN AIDS RELATED IMMUNODEFICIENCYR01AI029902 · NIAID · YALE UNIVERSITY · PI FLAVELL, RICHARD A · 1990 to 1994
–
NIAID NIH HHS 1 RO1 AI29902
6 · The paper itself

Abstract

Transcriptional factors of the NFAT family play an important role in regulating the expression of several cytokine genes during the immune response, such as the genes for interleukin 2 (IL-2) and IL-4, among others. Upon antigen stimulation, precursor CD4+ T helper (pTh) cells proliferate and differentiate into two populations of effector cells (eTh1 and eTh2), each one expressing a specific pattern of cytokines that distinguishes them from their precursors. eTh2 cells are the major source of IL-4, while gamma interferon is produced by eTh1 cells. Here we have used reporter transgenic mice to show that DNA binding and transcriptional activities of NFAT are transiently induced during the differentiation of pTh cells into either eTh1 or eTh2 cells to mediate the expression of IL-2 as a common growth factor in both pathways. However, although NFAT DNA binding is similarly induced in both eTh1 and eTh2 cells upon antigen stimulation, only the NFAT complexes present in eTh2 cells are able to mediate high-level transcription, and relatively little NFAT transcriptional activity was induced in eTh1 cells. In contrast to activated pTh cells, neither eTh1 nor eTh2 cells produced significant IL-2 upon stimulation, but the high levels of NFAT transcriptional activities directly correlate with the IL-4 production induced in response to antigen stimulation in eTh2 cells. These data suggest that activated NFAT is involved in the effector function of eTh2 cells and that the failure of eTh1 cells to produce IL-4 in response to an antigen is due, at least partially, to a failure to induce high-level transcription of the IL-4 gene by NFAT. Regulation of NFAT could be therefore a critical element in the polarization to eTh1 or eTh2.

Indexed as

Gene Expression RegulationNuclear ProteinsTranscriptional ActivationAnimalsCD4-Positive T-LymphocytesCell DifferentiationCell ExtractsCell NucleusCyclic AMP Response Element-Binding ProteinDNADNA-Binding ProteinsHumansInterleukin-4Jurkat CellsLymphocyte ActivationMiceCell ExtractsCyclic AMP Response Element-Binding ProteinDNADNA-Binding ProteinsInterleukin-4NFATC Transcription FactorsNuclear ProteinsTranscription Factor AP-1Transcription Factors

Identifiers

PMID9032280
PMCPMC231878
OpenAlexW2107412423

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.