Evidence map›Paper›PMID 21905024›Full record

ArticleEuropean journal of immunology2011

Persistence of IL-2 expressing Th17 cells in healthy humans and experimental autoimmune uveitis.

Cheng-Rong Yu, Hyun-Mee Oh, Nady Golestaneh, Ahjoku Amadi-Obi, Yun S Lee, Amarachi Eseonu, Rashid M Mahdi, Charles E Egwuagu

Open access · greenAbstract read
In one paragraph

Article in European journal of immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.7field-weighted citation impact, top 11% 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

17 citing papers in PubMed, 21 citations in OpenAlex.

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  7. The Common Cytokine Receptor γ Chain Family of Cytokines.Cold Spring Harbor perspectives in biology · 2018
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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

8 authors at 4 institutions in 2 countries.

Cheng-Rong YuMolecular Immunology Section, Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892-1857, USA.
Hyun-Mee Oh
Nady Golestaneh
Ahjoku Amadi-Obi
Yun S Lee
Amarachi Eseonu
Rashid M Mahdi
Charles E Egwuagu
National Eye Institute · USNational Institutes of Health · USGeorgetown University · USHarvard University · US

Funding

Mechanisms of immune homeostasis and regulation of intraocular inflammationZIAEY000372 · NEI · NATIONAL EYE INSTITUTE · PI EGWUAGU, CHARLES E · 2009 to 2025
$6.5M
Regulation of JAK/STAT pathways in the eyeZIAEY000315 · NEI · NATIONAL EYE INSTITUTE · PI EGWUAGU, CHARLES E · 2009 to 2025
$5.4M
Suppressor of Cytokine Signaling Regulates ProliferationZ01EY000372 · NEI · NATIONAL EYE INSTITUTE · PI EGWUAGU, CHARLES E · 2001 to 2008
$944k
Intramural NIH HHS Z01 EY000372
6 · The paper itself

Abstract

Compared with other T-helper subsets, Th17 cell numbers are very low in human blood but become elevated in chronic inflammatory diseases. In this study, we investigated mechanisms that may explain the frequent involvement of Th17 cells in autoimmune diseases such as uveitis. We compared Th17 and Th1 subsets and found that Th17 cells expressed lower IL-2 levels during Ag-priming and this correlated with their decreased susceptibility to activation-induced cell death (AICD). However, complete depletion of IL-2 with IL-2 neutralizing antibodies rendered Th17 cells as susceptible to apoptosis as Th1 cells, suggesting that the low levels of IL-2 produced by Th17 cells conferred survival advantages to this subset. We describe here a Th17 subtype that constitutively produces very low levels of IL-2 (Th17-DP). The Th17-DP population increased dramatically in the blood and retina of mice during experimental autoimmune uveitis, indicating their potential involvement in the etiology of uveitis. We further show that the majority of the memory Th17 cells in human blood are Th17-DP and are targets of daclizumab, an IL-2R antibody used in treating recalcitrant uveitis. Thus, Th17 cells may persist in tissues and contribute to chronic inflammation by limiting IL-2 production to levels that cannot provoke IL-2-induced AICD yet are sufficient to promote Th17 homeostatic expansion.

Indexed as

AnimalsAntibodiesAntibodies, Monoclonal, HumanizedAntibodies, NeutralizingAutoimmune DiseasesCell DeathDaclizumabHumansImmunoglobulin GInterleukin-2MiceMice, Inbred C57BLReceptors, Interleukin-2Th17 CellsTh1 CellsUveitisAntibodiesAntibodies, Monoclonal, HumanizedAntibodies, NeutralizingDaclizumabImmunoglobulin GInterleukin-2Receptors, Interleukin-2

Identifiers

PMID21905024
PMCPMC11305124
OpenAlexW2005955769

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Registered trials

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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.