Evidence map›Paper›PMID 35508809›Full record

ReviewNature reviews. Immunology2022

The immunology of multiple sclerosis.

Kathrine E Attfield, Lise Torp Jensen, Max Kaufmann, Manuel A Friese, Lars Fugger

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 209 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
209citing papers in PubMed, 4 pooled it
–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

209 citing papers in PubMed, 4 syntheses or guidelines pooled it.

  1. Pooled it
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  5. Trial
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  8. From danger to resolution: targeting purinergic signaling in CNS diseases.Medicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents · 2026
    Review
  9. B-cell targeting strategies for the treatment of multiple sclerosis: from non-cellular therapies to CAR-engineered cell therapies.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
    Review
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  15. Acta pharmaceutica Sinica. B · 2026
    Article
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149 more citing papers are in PubMed but not listed here.

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

5 authors.

Kathrine E AttfieldOxford Centre for Neuroinflammation, Nuffield Department of Clinical Neurosciences, Oxford University Hospitals, University of Oxford, Oxford, UK.
Lise Torp JensenDepartment of Clinical Medicine, Aarhus University Hospital, Aarhus, Denmark.
Max KaufmannInstitut für Neuroimmunologie und Multiple Sklerose, Zentrum für Molekulare Neurobiologie Hamburg, Universitätsklinikum Hamburg-Eppendorf, Hamburg, Germany.ORCID 0000-0002-1954-4425
Manuel A FrieseInstitut für Neuroimmunologie und Multiple Sklerose, Zentrum für Molekulare Neurobiologie Hamburg, Universitätsklinikum Hamburg-Eppendorf, Hamburg, Germany.ORCID 0000-0001-6380-2420
Lars FuggerOxford Centre for Neuroinflammation, Nuffield Department of Clinical Neurosciences, Oxford University Hospitals, University of Oxford, Oxford, UK. lars.fugger@ndcn.ox.ac.uk.ORCID 0000-0003-2883-3226

Funding

Medical Research Council MC_UU_00008/3Versus Arthritis 22933
6 · The paper itself

Abstract

Our incomplete understanding of the causes and pathways involved in the onset and progression of multiple sclerosis (MS) limits our ability to effectively treat this complex neurological disease. Recent studies explore the role of immune cells at different stages of MS and how they interact with cells of the central nervous system (CNS). The findings presented here begin to question the exclusivity of an antigen-specific cause and highlight how seemingly distinct immune cell types can share common functions that drive disease. Innovative techniques further expose new disease-associated immune cell populations and reinforce how environmental context is critical to their phenotype and subsequent role in disease. Importantly, the differentiation of immune cells into a pathogenic state is potentially reversible through therapeutic manipulation. As such, understanding the mechanisms that provide plasticity to causal cell types is likely key to uncoupling these disease processes and may identify novel therapeutic targets that replace the need for cell ablation.

Indexed as

Multiple SclerosisHumansPhenotype

Identifiers

What Socratic holds

Textmetadata
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 Socratic graph.