Evidence map›Paper›PMID 26172046›Full record

ArticlePloS one2015

Differences in CD44 Surface Expression Levels and Function Discriminates IL-17 and IFN-γ Producing Helper T Cells.

Julia Schumann, Katarina Stanko, Ulrike Schliesser, Christine Appelt, Birgit Sawitzki

Erratum issuedOpen access · goldAbstract readComparative Study
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

62 citing papers in PubMed, 89 citations in OpenAlex.

  1. Article
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  13. Pan-Variant SARS-CoV-2 Vaccines Induce Protective Immunity by Targeting Conserved Epitopes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
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  15. Frontiers in immunology · 2025
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  16. Theranostics · 2025
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2 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Julia SchumannInstitute of Medical Immunology, Charité University Medicine, Berlin, Germany.
Katarina StankoInstitute of Medical Immunology, Charité University Medicine, Berlin, Germany.
Ulrike SchliesserInstitute of Medical Immunology, Charité University Medicine, Berlin, Germany.
Christine AppeltInstitute of Medical Immunology, Charité University Medicine, Berlin, Germany.
Birgit SawitzkiInstitute of Medical Immunology, Charité University Medicine, Berlin, Germany; Berlin Brandenburg Center for Regenerative Therapies, Charité University Medicine, Berlin, Germany.
Charité - Universitätsmedizin Berlin · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CD44 is a prominent activation marker which distinguishes memory and effector T cells from their naïve counterparts. It also plays a role in early T cell signaling events as it is bound to the lymphocyte-specific protein kinase and thereby enhances T cell receptor signalling. Here, we investigated whether IFN-γ and IL-17 producing T helper cells differ in their CD44 expression and their dependence of CD44 for differentiation. Stimulation of CD4+ T cells with allogeneic dendritic cells resulted in the formation of three distinguishable populations: CD44+, CD44++ and CD44+++. In vitro and in vivo generated allo-reactive IL-17 producing T helper cells were mainly CD44+++ as compared to IFN-γ+ T helper cells, which were CD44++. This effect was enhanced under polarizing conditions. T helper 17 polarization led to a shift towards the CD44+++ population, whereas T helper 1 polarization diminished this population. Furthermore, blocking CD44 decreased IL-17 secretion, while IFN-γ was barely affected. Titration experiments revealed that low T cell receptor and CD28 stimulation supported T helper 17 rather than T helper 1 development. Under these conditions CD44 could act as a co-stimulatory molecule and replace CD28. Indeed, rested CD44+++CD4+ T cells contained already more total and especially phosphorylated zeta-chain-associated protein kinase 70 as compared to CD44++ cells. Our results support the notion, that CD44 enhances T cell receptor signaling strength by delivering lymphocyte-specific protein kinase, which is required for induction of IL-17 producing T helper cells.

Indexed as

Gene Expression RegulationAnimalsCD28 AntigensCD3 ComplexCD4-Positive T-LymphocytesDose-Response Relationship, DrugHumansHyaluronan ReceptorsInterferon-gammaInterleukin-17Intracellular SpaceMaleMiceReceptors, Antigen, T-CellSignal TransductionT-Lymphocytes, Helper-InducerCD28 AntigensCD3 ComplexHyaluronan ReceptorsInterferon-gammaInterleukin-17Receptors, Antigen, T-Cell

Identifiers

PMID26172046
PMCPMC4501817
OpenAlexW906352129

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.