Evidence map›Paper›PMID 28155899›Full record

ArticleScientific reports2017

Fingolimod alters the transcriptome profile of circulating CD4+ cells in multiple sclerosis.

Jörg Friess, Michael Hecker, Luisa Roch, Dirk Koczan, Brit Fitzner, Ines Charlotte Angerer, Ina Schröder, Kristin Flechtner, Hans-Jürgen Thiesen, Alexander Winkelmann and 1 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.4field-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

21 citing papers in PubMed, 38 citations in OpenAlex.

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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

11 authors at 2 institutions in 1 country.

Jörg FriessUniversity of Rostock, Department of Neurology, Division of Neuroimmunology, Gehlsheimer Str. 20, 18147 Rostock, Germany.
Michael HeckerUniversity of Rostock, Department of Neurology, Division of Neuroimmunology, Gehlsheimer Str. 20, 18147 Rostock, Germany.
Luisa RochUniversity of Rostock, Department of Neurology, Division of Neuroimmunology, Gehlsheimer Str. 20, 18147 Rostock, Germany.
Dirk KoczanSteinbeis Transfer Centre for Proteome Analysis, Schillingallee 70, 18057 Rostock, Germany.
Brit FitznerSteinbeis Transfer Centre for Proteome Analysis, Schillingallee 70, 18057 Rostock, Germany.
Ines Charlotte AngererUniversity of Rostock, Department of Neurology, Division of Neuroimmunology, Gehlsheimer Str. 20, 18147 Rostock, Germany.
Ina SchröderUniversity of Rostock, Department of Neurology, Division of Neuroimmunology, Gehlsheimer Str. 20, 18147 Rostock, Germany.
Kristin FlechtnerUniversity of Rostock, Institute of Immunology, Schillingallee 70, 18057 Rostock, Germany.
Hans-Jürgen ThiesenSteinbeis Transfer Centre for Proteome Analysis, Schillingallee 70, 18057 Rostock, Germany.
Alexander WinkelmannUniversity of Rostock, Department of Neurology, Division of Neuroimmunology, Gehlsheimer Str. 20, 18147 Rostock, Germany.
Uwe Klaus ZettlUniversity of Rostock, Department of Neurology, Division of Neuroimmunology, Gehlsheimer Str. 20, 18147 Rostock, Germany.
University of Rostock · DESteinbeis Foundation · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple sclerosis is a demyelinating disease affecting the central nervous system. T cells are known to contribute to this immune-mediated condition. Fingolimod modulates sphingosine-1-phosphate receptors, thereby preventing the egress of lymphocytes, especially CCR7-expressing CD8+ and CD4+ T cells, from lymphoid tissues. Using Affymetrix Human Transcriptome Arrays (HTA 2.0), we performed a transcriptome profiling analysis of CD4+ cells obtained from the peripheral blood of patients with highly active relapsing-remitting multiple sclerosis. The samples were drawn before the first administration of fingolimod as well as 24 hours and 3 months after the start of therapy. Three months after treatment initiation, 890 genes were found to be differentially expressed with fold-change >2.0 and t-test p-value < 0.001, among them several microRNA precursors. A subset of 272 genes were expressed at lower levels, including CCR7 as expected, while 618 genes showed an increase in expression, e.g., CCR2, CX3CR1, CD39, CD58 as well as LYN, PAK1 and TLR2. To conclude, we studied the gene expression of CD4+ cells to evaluate the effects of fingolimod treatment, and we identified 890 genes to be altered in expression after continuous drug administration. T helper cells circulating in the blood during fingolimod therapy present a distinct gene expression signature.

Indexed as

TranscriptomeAdultCD4-Positive T-LymphocytesCells, CulturedFemaleFingolimod HydrochlorideHumansImmunosuppressive AgentsMaleMiddle AgedMultiple SclerosisFingolimod HydrochlorideImmunosuppressive Agents

Identifiers

PMID28155899
PMCPMC5290459
OpenAlexW2583794702

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.