Evidence map›Paper›PMID 39468055›Full record

ArticleNature communications2024

Protective effect of TCR-mediated MAIT cell activation during experimental autoimmune encephalomyelitis.

Mark Walkenhorst, Jana K Sonner, Nina Meurs, Jan Broder Engler, Simone Bauer, Ingo Winschel, Marcel S Woo, Lukas Raich, Iris Winkler, Vanessa Vieira and 5 more

Abstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Review
  6. 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

15 authors.

Mark WalkenhorstInstitute of Neuroimmunology and Multiple Sclerosis, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.ORCID 0000-0002-2277-9532
Jana K SonnerInstitute of Neuroimmunology and Multiple Sclerosis, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.ORCID 0000-0002-4700-272X
Nina MeursInstitute of Neuroimmunology and Multiple Sclerosis, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.ORCID 0000-0001-5366-0123
Jan Broder EnglerInstitute of Neuroimmunology and Multiple Sclerosis, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.ORCID 0000-0002-3169-2076
Simone BauerInstitute of Neuroimmunology and Multiple Sclerosis, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Ingo WinschelInstitute of Neuroimmunology and Multiple Sclerosis, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.ORCID 0000-0001-9487-7070
Marcel S WooInstitute of Neuroimmunology and Multiple Sclerosis, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.ORCID 0000-0002-1306-2708
Lukas RaichInstitute of Neuroimmunology and Multiple Sclerosis, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Iris WinklerInstitute of Neuroimmunology and Multiple Sclerosis, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.ORCID 0000-0002-6900-5139
Vanessa VieiraInstitute of Neuroimmunology and Multiple Sclerosis, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Lisa UngerInstitute of Neuroimmunology and Multiple Sclerosis, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Gabriela SalinasNGS-Integrative Genomics Core Unit, Institute of Pathology, University Medical Center Göttingen, Göttingen, Germany.
Olivier LantzInstitut National de la Santé et de la Recherche Médicale U932, PSL University, Institut Curie, Paris, France.ORCID 0000-0003-3161-7719
Manuel A Friese *Institute of Neuroimmunology and Multiple Sclerosis, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. manuel.friese@zmnh.uni-hamburg.de.ORCID 0000-0001-6380-2420
Anne Willing *Institute of Neuroimmunology and Multiple Sclerosis, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. anne.willing@zmnh.uni-hamburg.de.ORCID 0000-0002-0924-2829

Funding

Bundesministerium für Bildung und Forschung (Federal Ministry of Education and Research) 01GI1605CDeutsche Forschungsgemeinschaft (German Research Foundation) Grant No. 470154978; WI 5322/2-1
6 · The paper itself

Abstract

Mucosal-associated invariant T (MAIT) cells express semi-invariant T cell receptors (TCR) for recognizing bacterial and yeast antigens derived from riboflavin metabolites presented on the non-polymorphic MHC class I-related protein 1 (MR1). Neuroinflammation in multiple sclerosis (MS) is likely initiated by autoreactive T cells and perpetuated by infiltration of additional immune cells, but the precise role of MAIT cells in MS pathogenesis remains unknown. Here, we use experimental autoimmune encephalomyelitis (EAE), a mouse model of MS, and find an accumulation of MAIT cells in the inflamed central nervous system (CNS) enriched for MAIT17 (RORγt

Indexed as

Encephalomyelitis, Autoimmune, ExperimentalLymphocyte ActivationMice, Inbred C57BLMucosal-Associated Invariant T CellsReceptors, Antigen, T-CellAnimalsCentral Nervous SystemCytokinesFemaleHistocompatibility Antigens Class IMiceMinor Histocompatibility AntigensMultiple SclerosisNuclear Receptor Subfamily 1, Group F, Member 3RibitolUracil5-(2-oxopropylideneamino)-6-d-ribitylaminouracilCytokinesHistocompatibility Antigens Class IMinor Histocompatibility AntigensNuclear Receptor Subfamily 1, Group F, Member 3Receptors, Antigen, T-CellRibitolUracil

Identifiers

PMID39468055
PMCPMC11519641

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.