Evidence map›Paper›PMID 29314605›Full record

ArticleCNS neuroscience & therapeutics2018

Transcriptome profiling of peripheral blood immune cell populations in multiple sclerosis patients before and during treatment with a sphingosine-1-phosphate receptor modulator.

Ines C Angerer, Michael Hecker, Dirk Koczan, Luisa Roch, Jörg Friess, Annelen Rüge, Brit Fitzner, Nina Boxberger, Ina Schröder, Kristin Flechtner and 4 more

Abstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
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

15 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Fingolimod Therapy in Multiple Sclerosis Leads to the Enrichment of a Subpopulation of Aged NK Cells.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021
    Article
  7. Review
  8. Review
  9. Article
  10. Article
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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

14 authors.

Ines C AngererDepartment of Neurology, Division of Neuroimmunology, University of Rostock, Rostock, Germany.
Michael HeckerDepartment of Neurology, Division of Neuroimmunology, University of Rostock, Rostock, Germany.ORCID 0000-0001-7015-3094
Dirk KoczanSteinbeis Transfer Center for Proteome Analysis, Rostock, Germany.
Luisa RochDepartment of Neurology, Division of Neuroimmunology, University of Rostock, Rostock, Germany.
Jörg FriessDepartment of Neurology, Division of Neuroimmunology, University of Rostock, Rostock, Germany.
Annelen RügeDepartment of Neurology, Division of Neuroimmunology, University of Rostock, Rostock, Germany.
Brit FitznerDepartment of Neurology, Division of Neuroimmunology, University of Rostock, Rostock, Germany.
Nina BoxbergerDepartment of Neurology, Division of Neuroimmunology, University of Rostock, Rostock, Germany.
Ina SchröderDepartment of Neurology, Division of Neuroimmunology, University of Rostock, Rostock, Germany.
Kristin FlechtnerInstitute of Immunology, University of Rostock, Rostock, Germany.
Hans-Jürgen ThiesenSteinbeis Transfer Center for Proteome Analysis, Rostock, Germany.
Alexander WinkelmannDepartment of Neurology, Division of Neuroimmunology, University of Rostock, Rostock, Germany.
Stefanie MeisterDepartment of Neurology, Division of Neuroimmunology, University of Rostock, Rostock, Germany.
Uwe K ZettlDepartment of Neurology, Division of Neuroimmunology, University of Rostock, Rostock, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsFingolimod is a sphingosine-1-phosphate (S1P) receptor modulator approved for the treatment of the relapsing form of multiple sclerosis (MS). It prevents the egress of lymphocyte subpopulations from lymphoid tissues into the circulation. Here, we explored the broad effects of fingolimod on gene expression in different immune cell subsets.

methodsUtilizing 150 high-resolution microarrays from Affymetrix, we obtained the transcriptome profiles of 5 cell populations, which were separated from the peripheral blood of MS patients prior to and following oral administration of fingolimod.

resultsAfter 3 months of treatment, significant transcriptome shifts were seen in CD4+ and CD8+ cells, which is mainly attributable to the selective homing of naive T cells and central memory T cells. Although the number of B cells was greatly reduced in the blood of fingolimod-treated MS patients, the analysis of differential expression in CD19+ cells identified only a small set of 42 genes, which indicated a slightly higher frequency of transitional B cells. The transcriptome signatures of CD14+ monocytes and CD56+ natural killer cells were not affected.

conclusionOur study corroborates changes in the composition of circulating immune cells in response to fingolimod and delineates the respective implications at the RNA level. Our data may be valuable for comparing the effects of novel S1P receptor modulating agents, which may be a therapeutic option for patients with secondary progressive MS as well.

Indexed as

Administration, OralAdultFingolimod HydrochlorideGene Expression ProfilingHumansImmunosuppressive AgentsLymphocytesMiddle AgedMultiple SclerosisReceptors, LysosphingolipidFingolimod HydrochlorideImmunosuppressive AgentsReceptors, LysosphingolipidCD19+ B cellsfingolimod therapyperipheral bloodrelapsing-remitting multiple sclerosistranscriptome microarray analysis

Identifiers

PMID29314605
PMCPMC6490155

What OpenQuestion holds

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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.