Evidence map›Paper›PMID 26637427›Full record

ArticleActa neuropathologica communications2015

Autoimmune encephalitis in humans: how closely does it reflect multiple sclerosis ?

Romana Höftberger, Marianne Leisser, Jan Bauer, Hans Lassmann

Open access · goldAbstract readCase Reports
In one paragraph

Article in Acta neuropathologica communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

17 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Review
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  4. Kurt Jellinger 90: his contribution to neuroimmunology.Journal of neural transmission (Vienna, Austria : 1996) · 2021
    Review
  5. Article
  6. Review
  7. Article
  8. Neuroinflammation: 2021 update.Free neuropathology · 2021
    Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Acute disseminated encephalomyelitis in an elderly patient.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2017
    Article
  14. Review
  15. Review
  16. Review
  17. 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

4 authors at 1 institution in 1 country.

Romana HöftbergerInstitute of Neurology, Medical University of Vienna, Vienna, Austria.
Marianne LeisserCenter for Brain Research, Medical University of Vienna, Vienna, Austria.
Jan BauerCenter for Brain Research, Medical University of Vienna, Vienna, Austria.
Hans LassmannCenter for Brain Research, Medical University of Vienna, Vienna, Austria. hans.lassmann@meduniwien.ac.at.
Medical University of Vienna · AT

Funding

Austrian Science Fund FWF I 2114
6 · The paper itself

Abstract

introductionMultiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system. Immunological studies suggest that it is a T-cell mediated autoimmune disease, although an MS-specific target antigen for autoimmunity has so far not been identified. Models of experimental autoimmune encephalomyelitis in part reproduce features of MS, but none of the models so far covers the entire spectrum of pathology and immunology. Autoimmune disease of the nervous system has occasionally been observed in humans after active sensitization with brain tissue or brain cells, giving rise to acute demyelinating polyradiculoneuritis, acute disseminated encephalomyelitis and in rare cases reflecting an inflammatory demyelinating condition similar to acute multiple sclerosis. In this study we analyzed in detail the immunopathology in archival autopsy tissue of a patient who died with an MS like disease after repeated exposure to subcutaneous injections of lyophilized brain cells.

resultsThe pathology of this patient fulfilled all pathological diagnostic criteria of MS. Demyelination and tissue injury was associated with antibody (IgM) deposition at active lesion sites and complement activation. Major differences to classical EAE models were seen in the composition of inflammatory infiltrates, being dominated by B-cells, infiltration of IgM positive plasma cells, profound infiltration of the tissue by CD8(+) T-lymphocytes and a nearly complete absence of CD4(+) T-cells.

conclusionsOur study shows that auto-sensitization of humans with brain tissue can induce a disease, which closely reflects the pathology of MS, but that the mechanisms leading to demyelination and tissue injury differ from those, generally implicated in the pathophysiology of MS through studies in experimental autoimmune encephalomyelitis.

Indexed as

Antigens, CDAntigens, Differentiation, MyelomonocyticAutopsyB-LymphocytesBrainCalcium-Binding ProteinsCD68 MoleculeDNA-Binding ProteinsEncephalitisHashimoto DiseaseHumansMaleMicrofilament ProteinsMiddle AgedMultiple SclerosisNerve Tissue ProteinsAIF1 protein, humanAntigens, CDAntigens, Differentiation, MyelomonocyticCalcium-Binding ProteinsCD68 antigen, humanCD68 MoleculeDNA-Binding ProteinsMicrofilament ProteinsMYT1 protein, humanNerve Tissue ProteinsTranscription Factors

Identifiers

PMID26637427
PMCPMC4670499
OpenAlexW2189083018

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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.