Evidence map›Paper›PMID 32503977›Full record

ArticleNature communications2020

Transcriptomics and proteomics reveal a cooperation between interferon and T-helper 17 cells in neuromyelitis optica.

Agnieshka M Agasing, Qi Wu, Bhuwan Khatri, Nadja Borisow, Klemens Ruprecht, Alexander Ulrich Brandt, Saurabh Gawde, Gaurav Kumar, James L Quinn, Rose M Ko and 4 more

Registry-linked trialOpen access · goldAbstract read
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05245344 (Effects of Ozanimod on Immune-mediated Mechanisms of Neurodegeneration in Multiple Sclerosis - a Preclinical Study), which is not on this map. Cited by 56 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 1 pooled it
8.4field-weighted citation impact, top 2% 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.

NCT05245344 unknown statusnot on this mapstarted 2022, after this paper: background citation

Effects of Ozanimod on Immune-mediated Mechanisms of Neurodegeneration in Multiple Sclerosis - a Preclinical Study

TypeobservationalSponsorNeuromed IRCCSRan2022 to 2023Enrolled154ConditionsRelapsing-Remitting Multiple Sclerosis (RRMS), Neuromyelitis Optica, HealthyArmsPeripheral blood withdrawal
3 · Its place in the literature

Who cites it

56 citing papers in PubMed, 1 synthesis or guideline pooled it, 96 citations in OpenAlex.

  1. Pooled it
  2. Observational
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Type I Interferon Signaling Augments Autoimmunity in Neuromyelitis Optica Spectrum Disorder.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article
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 at 5 institutions in 2 countries.

Agnieshka M AgasingArthritis and Clinical Immunology Research Program, Oklahoma Medical Research Foundation, 825 NE 13th St, Oklahoma City, OK, 73104, USA.
Qi WuDepartment of Neurology, University of Michigan Medical School, 109 Zina Pitcher Place, Biomedical Research Building Room 4258, Ann Arbor, MI, 48109, USA.
Bhuwan KhatriGenes and Human Disease Research Program, Oklahoma Medical Research Foundation, 825 NE 13th St, Oklahoma City, OK, 73104, USA.
Nadja BorisowNeuroCure Clinical Research Center and Experimental and Clinical Research Center, Max Delbrueck Center for Molecular Medicine and Charité Universitätsmedizin, Lindenberger Weg 80, 13125, Berlin, Germany.
Klemens RuprechtDepartment of Neurology with Experimental Neurology, Charité Universitätsmedizin, Charitéplatz 1, Berlin, 10117, Germany.ORCID http://orcid.org/0000-0003-1962-6014
Alexander Ulrich BrandtNeuroCure Clinical Research Center and Experimental and Clinical Research Center, Max Delbrueck Center for Molecular Medicine and Charité Universitätsmedizin, Lindenberger Weg 80, 13125, Berlin, Germany.
Saurabh GawdeArthritis and Clinical Immunology Research Program, Oklahoma Medical Research Foundation, 825 NE 13th St, Oklahoma City, OK, 73104, USA.
Gaurav KumarArthritis and Clinical Immunology Research Program, Oklahoma Medical Research Foundation, 825 NE 13th St, Oklahoma City, OK, 73104, USA.
James L QuinnArthritis and Clinical Immunology Research Program, Oklahoma Medical Research Foundation, 825 NE 13th St, Oklahoma City, OK, 73104, USA.
Rose M KoArthritis and Clinical Immunology Research Program, Oklahoma Medical Research Foundation, 825 NE 13th St, Oklahoma City, OK, 73104, USA.
Yang Mao-DraayerDepartment of Neurology, University of Michigan Medical School, 109 Zina Pitcher Place, Biomedical Research Building Room 4258, Ann Arbor, MI, 48109, USA.ORCID http://orcid.org/0000-0001-6248-3480
Christopher J LessardGenes and Human Disease Research Program, Oklahoma Medical Research Foundation, 825 NE 13th St, Oklahoma City, OK, 73104, USA.
Friedemann PaulNeuroCure Clinical Research Center and Experimental and Clinical Research Center, Max Delbrueck Center for Molecular Medicine and Charité Universitätsmedizin, Lindenberger Weg 80, 13125, Berlin, Germany.
Robert C AxtellArthritis and Clinical Immunology Research Program, Oklahoma Medical Research Foundation, 825 NE 13th St, Oklahoma City, OK, 73104, USA. Bob-Axtell@omrf.org.ORCID http://orcid.org/0000-0002-1435-4753
Oklahoma Medical Research Foundation · USMax Delbrück Center · DEUniversity of Michigan · USCharité - Universitätsmedizin Berlin · DEUniversity of California, Irvine · US

Funding

Understanding the roles type I Interferon and TH17 play in Neuromyelitis Optica and other autoimmune diseases.R01AI137047 · NIAID · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI AXTELL, ROBERT C · 2018 to 2021
$2.8M
Pathogenic B cell and T helper cell interactions in Neuromyelitis OpticaR01EY027346 · NEI · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI AXTELL, ROBERT C · 2017 to 2021
$2.2M
NEI NIH HHS R01 EY027346NIAID NIH HHS R01 AI137047
6 · The paper itself

Abstract

Type I interferon (IFN-I) and T helper 17 (TH17) drive pathology in neuromyelitis optica spectrum disorder (NMOSD) and in TH17-induced experimental autoimmune encephalomyelitis (TH17-EAE). This is paradoxical because the prevalent theory is that IFN-I inhibits TH17 function. Here we report that a cascade involving IFN-I, IL-6 and B cells promotes TH17-mediated neuro-autoimmunity. In NMOSD, elevated IFN-I signatures, IL-6 and IL-17 are associated with severe disability. Furthermore, IL-6 and IL-17 levels are lower in patients on anti-CD20 therapy. In mice, IFN-I elevates IL-6 and exacerbates TH17-EAE. Strikingly, IL-6 blockade attenuates disease only in mice treated with IFN-I. By contrast, B-cell-deficiency attenuates TH17-EAE in the presence or absence of IFN-I treatment. Finally, IFN-I stimulates B cells to produce IL-6 to drive pathogenic TH17 differentiation in vitro. Our data thus provide an explanation for the paradox surrounding IFN-I and TH17 in neuro-autoimmunity, and may have utility in predicting therapeutic response in NMOSD.

Indexed as

AdultAnimalsAutoimmunityB-LymphocytesEncephalomyelitis, Autoimmune, ExperimentalFemaleGene Expression ProfilingHumansInterferon Type IInterleukin-17Interleukin-6MaleMiceMiddle AgedNeuromyelitis OpticaProteomicsIL6 protein, humanInterferon Type IInterleukin-17Interleukin-6interleukin-6, mouse

Identifiers

PMID32503977
PMCPMC7275086
OpenAlexW3033198321

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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.