Evidence map›Paper›PMID 19801513›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2009

PU.1 regulates TCR expression by modulating GATA-3 activity.

Hua-Chen Chang, Ling Han, Rukhsana Jabeen, Sebastian Carotta, Stephen L Nutt, Mark H Kaplan

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

42 citing papers in PubMed, 67 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. T helper 2 cells in asthma.The Journal of experimental medicine · 2023
    Review
  5. Article
  6. Article
  7. Article
  8. Expression profile of PU.1 in CD4Clinical and experimental medicine · 2021
    Article
  9. Cigarette smoke induction of S100A9 contributes to chronic obstructive pulmonary disease.American journal of physiology. Lung cellular and molecular physiology · 2020
    Article
  10. Review
  11. Article
  12. Review
  13. Effects of allergic stimulation and glucocorticoids on miR-155 in CD4American journal of clinical and experimental immunology · 2018
    Article
  14. Article
  15. Review
  16. Article
  17. The transcription factor network in Th9 cells.Seminars in immunopathology · 2017
    Review
  18. Review
  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

6 authors at 2 institutions in 2 countries.

Hua-Chen ChangDepartment of Pediatrics, Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Ling Han
Rukhsana Jabeen
Sebastian Carotta
Stephen L Nutt
Mark H Kaplan
Walter and Eliza Hall Institute of Medical Research · AUIndiana University School of Medicine

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
NIAID NIH HHS AI057459NIAID NIH HHS R01 AI057459
6 · The paper itself

Abstract

The Ets transcription factor PU.1 is a master regulator for the development of multiple lineages during hematopoiesis. The expression pattern of PU.1 is dynamically regulated during early T lineage development in the thymus. We previously revealed that PU.1 delineates heterogeneity of effector Th2 populations. In this study, we further define the function of PU.1 on the Th2 phenotype using mice that specifically lack PU.1 in T cells using an lck-Cre transgene with a conditional Sfpi1 allele (Sfpi1(lck-/-)). Although deletion of PU.1 by the lck-Cre transgene does not affect T cell development, Sfpi1(lck-/-) T cells have a lower activation threshold than wild-type T cells. When TCR engagement is limiting, Sfpi1(lck-/-) T cells cultured in Th2 polarizing conditions secrete higher levels of Th2 cytokines and have greater cytokine homogeneity than wild-type cells. We show that PU.1 modulates the levels of TCR expression in CD4(+) T cells by regulating the DNA-binding activity of GATA-3 and limiting GATA-3 regulation of TCR gene expression. GATA-3-dependent regulation of TCR expression is also observed in Th1 and Th2 cells. In CD4(+) T cells, PU.1 expression segregates into subpopulations of cells that have lower levels of surface TCR, suggesting that PU.1 contributes to the heterogeneity of TCR expression. Thus, we have identified a mechanism whereby increased GATA-3 function in the absence of the antagonizing activity of PU.1 leads to increased TCR expression, a reduced activation threshold, and increased homogeneity in Th2 populations.

Indexed as

AnimalsCD4-Positive T-LymphocytesCell DifferentiationCytokinesFemaleGATA3 Transcription FactorGene Knockdown TechniquesMiceMice, Inbred C57BLMice, TransgenicProto-Oncogene ProteinsProto-Oncogene Protein Spi-1Receptors, Antigen, T-CellRNA, Small InterferingTh2 CellsTrans-ActivatorsCytokinesGata3 protein, mouseGATA3 Transcription FactorProto-Oncogene ProteinsProto-Oncogene Protein Spi-1Receptors, Antigen, T-CellRNA, Small InterferingTrans-Activators

Identifiers

PMID19801513
PMCPMC2768261
OpenAlexW2124457673

What OpenQuestion holds

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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.