Evidence map›Paper›PMID 23365462›Full record

ArticleBlood2013

Differential control of Helios(+/-) Treg development by monocyte subsets through disparate inflammatory cytokines.

Hui Zhong, Karina Yazdanbakhsh

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

20 citing papers in PubMed, 31 citations in OpenAlex.

  1. Trial
  2. Hemin controls T cell polarization in sickle cell alloimmunization.Journal of immunology (Baltimore, Md. : 1950) · 2014
    Trial
  3. Review
  4. Review
  5. Coexpression of Helios in Foxp3Disease markers · 2021
    Review
  6. Article
  7. Article
  8. Foxp3BMC immunology · 2019
    Article
  9. Article
  10. Molecular mechanisms underlying Th1-like Treg generation and function.Cellular and molecular life sciences : CMLS · 2017
    Review
  11. Immunoregulatory networks in sickle cell alloimmunization.Hematology. American Society of Hematology. Education Program · 2016
    Review
  12. The Ikaros family of zinc-finger proteins.Acta pharmaceutica Sinica. B · 2016
    Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. 'Hardcore' OX40Oncoimmunology
    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 1 institution in 1 country.

Hui ZhongLaboratory of Complement Biology, New York Blood Center, New York, NY 10065, USA.
Karina Yazdanbakhsh
New York Blood Center · US

Funding

Immunoregulatory responses in patients with ITPR01HL096497 · NHLBI · NEW YORK BLOOD CENTER · PI YAZDANBAKHSH, KARINA · 2009 to 2012
$1.6M
NHLBI NIH HHS R01 HL096497NHLBI NIH HHS R01 HL096497-01
6 · The paper itself

Abstract

Foxp3(+) regulatory T cells (Tregs) play a pivotal role in control of autoimmunity and pathological immune responses. Helios, the Ikarus family transcription factor, binds to the Foxp3 promoter, stabilizing its expression, and is expressed in 70% of peripheral Tregs of healthy individuals. This frequency is altered during malignancy, infection, and autoimmunity, although the mechanisms that control proliferation and relative numbers of Helios(+/-) Tregs remain largely unknown. Using a T-cell-monocyte in vitro stimulation assay, we now show that proliferation of Helios(+) Tregs is inhibited by CD16(+) monocyte subset. Antibody blocking with anti-interleukin (IL)-12 reversed this inhibition, whereas addition of IL-12 suppressed Helios(+) Treg expansion, indicating that CD16(+) monocyte control of Helios(+) Treg numbers is mediated through IL-12. In contrast, proliferation of Helios(-) Tregs, which express higher levels of tumor necrosis factor receptor II (TNFRII), was suppressed by TNF-α, whereas anti-TNF-α and anti-TNFRII reversed the inhibition. CD16(-) monocyte subset was mainly responsible for TNF-α-mediated control of Helios(-) Treg expansion. Altogether, these data suggest a differential role for monocyte subsets in control of Helios(+/-) Treg development that is mediated by distinct inflammatory cytokines. These data may have important implications for understanding the pathogenesis as well as control of chronic inflammatory and autoimmune diseases.

Indexed as

Cell DifferentiationCell ProliferationCells, CulturedCoculture TechniquesCytokinesGPI-Linked ProteinsHeterozygoteHumansIkaros Transcription FactorInflammation MediatorsInterleukin-12LymphopoiesisMonocytesReceptors, IgGT-Lymphocytes, RegulatoryTumor Necrosis Factor-alphaCytokinesFCGR3B protein, humanGPI-Linked ProteinsIkaros Transcription FactorIKZF2 protein, humanInflammation MediatorsInterleukin-12Receptors, IgGTumor Necrosis Factor-alpha

Identifiers

PMID23365462
PMCPMC3612859
OpenAlexW2008257992

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.