Evidence map›Paper›PMID 34381335›Full record

ArticleFrontiers in cellular neuroscience2021

Decreased Neurofilament L Chain Levels in Cerebrospinal Fluid and Tolerogenic Plasmacytoid Dendritic Cells in Natalizumab-Treated Multiple Sclerosis Patients - Brief Research Report.

Adriel S Moraes, Vinicius O Boldrini, Alliny C Dionete, Marilia D Andrade, Ana Leda F Longhini, Irene Santos, Amanda D R Lima, Veronica A P G Silva, Rafael P C Dias Carneiro, Raphael P S Quintiliano and 12 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in cellular neuroscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

3 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Review
  3. 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

22 authors at 3 institutions in 2 countries.

Adriel S MoraesNeuroimmunology Unit, Department of Genetics, Evolution, Microbiology, and Immunology, University of Campinas (UNICAMP), Campinas, Brazil.
Vinicius O BoldriniNeuroimmunology Unit, Department of Genetics, Evolution, Microbiology, and Immunology, University of Campinas (UNICAMP), Campinas, Brazil.
Alliny C DioneteNeuroimmunology Unit, Department of Genetics, Evolution, Microbiology, and Immunology, University of Campinas (UNICAMP), Campinas, Brazil.
Marilia D AndradeNeuroimmunology Unit, Department of Genetics, Evolution, Microbiology, and Immunology, University of Campinas (UNICAMP), Campinas, Brazil.
Ana Leda F LonghiniNeuroimmunology Unit, Department of Genetics, Evolution, Microbiology, and Immunology, University of Campinas (UNICAMP), Campinas, Brazil.
Irene SantosNeuroimmunology Unit, Department of Genetics, Evolution, Microbiology, and Immunology, University of Campinas (UNICAMP), Campinas, Brazil.
Amanda D R LimaNeuroimmunology Unit, Department of Genetics, Evolution, Microbiology, and Immunology, University of Campinas (UNICAMP), Campinas, Brazil.
Veronica A P G SilvaNeuroimmunology Unit, Department of Genetics, Evolution, Microbiology, and Immunology, University of Campinas (UNICAMP), Campinas, Brazil.
Rafael P C Dias CarneiroNeuroimmunology Unit, Department of Genetics, Evolution, Microbiology, and Immunology, University of Campinas (UNICAMP), Campinas, Brazil.
Raphael P S QuintilianoNeuroimmunology Unit, Department of Genetics, Evolution, Microbiology, and Immunology, University of Campinas (UNICAMP), Campinas, Brazil.
Breno B FerrariNeuroimmunology Unit, Department of Genetics, Evolution, Microbiology, and Immunology, University of Campinas (UNICAMP), Campinas, Brazil.
Alfredo DamascenoDepartment of Neurology, University of Campinas, Campinas, Brazil.
Fernando PradellaNeuroimmunology Unit, Department of Genetics, Evolution, Microbiology, and Immunology, University of Campinas (UNICAMP), Campinas, Brazil.
Alessandro S FariasNeuroimmunology Unit, Department of Genetics, Evolution, Microbiology, and Immunology, University of Campinas (UNICAMP), Campinas, Brazil.
Charles P TilberyMS Clinic of Santa Casa de São Paulo (CATEM), São Paulo, Brazil.
Renan B DominguesMS Clinic of Santa Casa de São Paulo (CATEM), São Paulo, Brazil.
Carlos SenneSenne Liquor Diagnóstico, São Paulo, Brazil.
Gustavo B P FernandesSenne Liquor Diagnóstico, São Paulo, Brazil.
Felipe von GlehnNeuroimmunology Unit, Department of Genetics, Evolution, Microbiology, and Immunology, University of Campinas (UNICAMP), Campinas, Brazil.
Carlos Otavio BrandãoNeuroimmunology Unit, Department of Genetics, Evolution, Microbiology, and Immunology, University of Campinas (UNICAMP), Campinas, Brazil.
Carla R A V StellaDepartment of Neurology, University of Campinas, Campinas, Brazil.
Leonilda M B SantosNeuroimmunology Unit, Department of Genetics, Evolution, Microbiology, and Immunology, University of Campinas (UNICAMP), Campinas, Brazil.
Universidade Estadual de Campinas (UNICAMP) · BRHospital Israelita Albert Einstein · BRUniversity of Alabama at Birmingham · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNeurofilament Light (NfL) chain levels in both cerebrospinal fluid (CSF) and serum have been correlated with the reduction of axonal damage in multiple sclerosis (MS) patients treated with Natalizumab (NTZ). However, little is known about the function of plasmacytoid cells in NTZ-treated MS patients.

objectiveTo evaluate CSF NfL, serum levels of soluble-HLA-G (sHLA-G), and eventual tolerogenic behavior of plasmacytoid dendritic cells (pDCs) in MS patients during NTZ treatment.

methodsCSF NfL and serum sHLA-G levels were measured using an ELISA assay, while pDCs (BDCA-2

resultsCSF levels of NfL were significantly reduced during NTZ treatment, while the serum levels of sHLA-G were increased. Moreover, NTZ treatment enhanced tolerogenic (HLA-G

conclusionThese findings suggest that NTZ stimulates the production of molecules with immunoregulatory function such as HLA-G and CD274 programmed death-ligand 1 (PD-L1) which may contribute to the reduction of axonal damage represented by the decrease of NfL levels in patients with MS.

Indexed as

cerebrospinal fluidHLA-DRHLA-Gneurofilament light chainneuroinflammationPD-L1

Identifiers

PMID34381335
PMCPMC8350727
OpenAlexW3184316109

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.