Evidence map›Paper›PMID 26062998›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2015

Eos Is Redundant for Regulatory T Cell Function but Plays an Important Role in IL-2 and Th17 Production by CD4+ Conventional T Cells.

Sadiye Amcaoglu Rieder, Amina Metidji, Deborah Dacek Glass, Angela M Thornton, Tohru Ikeda, Bruce A Morgan, Ethan M Shevach

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

27 citing papers in PubMed, 50 citations in OpenAlex.

  1. Aiolos and Eos drive distinct human TH17 functional states.Cellular and molecular life sciences : CMLS · 2026
    Article
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  20. Regulatory T Cell Development in the Thymus.Journal of immunology (Baltimore, Md. : 1950) · 2019
    Review
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.

Sadiye Amcaoglu RiederLaboratory of Immunology, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892; and.
Amina MetidjiLaboratory of Immunology, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892; and.
Deborah Dacek GlassLaboratory of Immunology, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892; and.
Angela M ThorntonLaboratory of Immunology, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892; and.
Tohru IkedaCutaneous Biology Research Center, Department of Dermatology, Harvard Medical School and Massachusetts General Hospital, Boston, MA 02129.
Bruce A MorganCutaneous Biology Research Center, Department of Dermatology, Harvard Medical School and Massachusetts General Hospital, Boston, MA 02129.
Ethan M ShevachLaboratory of Immunology, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892; and eshevach@niaid.nih.gov.
National Institute of Allergy and Infectious Diseases · USMassachusetts General Hospital · US

Funding

Studies of the Function of Naturally Occurring and Adaptive T Regulatory CellsZIAAI000959 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI SHEVACH, ETHAN · 2009 to 2025
$17.6M
Studies of the Function of Naturally Occurring and Adaptive T Regulatory CellsZ01AI000959 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI SHEVACH, ETHAN M. · 2006 to 2008
$5.1M
Inductive properties of the dermal papilla of the hair follicleR01AR055256 · NIAMS · MASSACHUSETTS GENERAL HOSPITAL · PI MORGAN, BRUCE A · 2007 to 2016
$3.9M
The Helios Gene in Development and Homeostasis of SkinR01AR052339 · NIAMS · MASSACHUSETTS GENERAL HOSPITAL · PI MORGAN, BRUCE A · 2007 to 2009
$1.1M
Intramural NIH HHS Z01 AI000959NIAMS NIH HHS R01 AR052339NIAMS NIH HHS R01 AR055256
6 · The paper itself

Abstract

Eos belongs to the Ikaros family of transcription factors. It was reported to be a regulatory T cell (Treg) signature gene, to play a critical role in Treg suppressor functions, and to maintain Treg stability. We used mice with a global deficiency in Eos to re-examine the role of Eos expression in both Tregs and conventional T cells (Tconvs). Tregs from Eos-deficient (Eos(-/-)) mice developed normally, displayed a normal Treg phenotype, and exhibited normal suppressor function in vitro. Eos(-/-) Tregs were as effective as Tregs from wild-type (WT) mice in suppressing inflammation in a model of inflammatory bowel disease. Bone marrow (BM) from Eos(-/-) mice was as effective as that from WT mice in controlling T cell activation when used to reconstitute immunodeficient mice in the presence of scurfy fetal liver cells. Surprisingly, Eos was expressed in activated Tconvs and was required for IL-2 production, CD25 expression, and proliferation in vitro by CD4(+) Tconvs. Eos(-/-) mice developed more severe experimental autoimmune encephalomyelitis than WT mice, displayed increased numbers of effector T cells in the periphery and CNS, and amplified IL-17 production. In conclusion, our studies are not consistent with a role for Eos in Treg development and function but demonstrate that Eos plays an important role in the activation and differentiation of Tconvs.

Indexed as

AnimalsBone Marrow CellsCarrier ProteinsCell DifferentiationCell ProliferationDisease Models, AnimalDNA-Binding ProteinsEncephalomyelitis, Autoimmune, ExperimentalGene Expression Regulation, DevelopmentalHumansInflammatory Bowel DiseasesInterleukin-17Interleukin-2Interleukin-2 Receptor alpha SubunitLymphocyte ActivationMiceCarrier ProteinsDNA-Binding ProteinsInterleukin-17Interleukin-2Interleukin-2 Receptor alpha SubunitNerve Tissue ProteinsZfpn1a4 protein, mouse

Identifiers

PMID26062998
PMCPMC4491037
OpenAlexW1542676327

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.