Evidence map›Paper›PMID 34145056›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2021

Complex Autoantibody Responses Occur following Moderate to Severe Traumatic Brain Injury.

Edward J Needham, Oda Stoevesandt, Eric P Thelin, Henrik Zetterberg, Elisa R Zanier, Faiez Al Nimer, Nicholas J Ashton, Joanne G Outtrim, Virginia F J Newcombe, Hani S Mousa and 11 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

32 citing papers in PubMed, 55 citations in OpenAlex.

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  12. Immune Response in Traumatic Brain Injury.Current neurology and neuroscience reports · 2024
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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

21 authors at 8 institutions in 6 countries.

Edward J NeedhamDepartment of Clinical Neurosciences, University of Cambridge, United Kingdom; edneedham@doctors.org.uk.
Oda StoevesandtCambridge Protein Arrays Ltd., Cambridge, United Kingdom.
Eric P ThelinDepartment of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.ORCID 0000-0002-2338-4364
Henrik ZetterbergDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Elisa R ZanierDipartimento di Ricerca Neuroscienze, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Milan, Italy.ORCID 0000-0002-3011-8718
Faiez Al NimerDepartment of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
Nicholas J AshtonDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Joanne G OuttrimDivision of Anaesthesia, Department of Medicine, University of Cambridge, United Kingdom.ORCID 0000-0001-8118-6430
Virginia F J NewcombeDivision of Anaesthesia, Department of Medicine, University of Cambridge, United Kingdom.ORCID 0000-0001-6044-9035
Hani S MousaDepartment of Clinical Neurosciences, University of Cambridge, United Kingdom.ORCID 0000-0002-8327-7114
Joel SimrénDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.ORCID 0000-0001-5081-6604
Kaj BlennowDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Zhihui YangProgram for Neurotrauma, Neuroproteomics and Biomarker Research, Departments of Emergency Medicine, Psychiatry and Neuroscience, University of Florida, McKnight Brain Institute.
Peter J HutchinsonDivision of Academic Neurosurgery, Department of Clinical Neurosciences, University of Cambridge, Cambridge, United Kingdom.
Fredrik PiehlDepartment of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
Adel E HelmyDivision of Academic Neurosurgery, Department of Clinical Neurosciences, University of Cambridge, Cambridge, United Kingdom.ORCID 0000-0002-0531-0556
Mike J TaussigCambridge Protein Arrays Ltd., Cambridge, United Kingdom.
Kevin K W WangProgram for Neurotrauma, Neuroproteomics and Biomarker Research, Departments of Emergency Medicine, Psychiatry and Neuroscience, University of Florida, McKnight Brain Institute.ORCID 0000-0002-9343-6473
Joanne L JonesDepartment of Clinical Neurosciences, University of Cambridge, United Kingdom.ORCID 0000-0003-4974-1371
David K MenonDivision of Anaesthesia, Department of Medicine, University of Cambridge, United Kingdom.ORCID 0000-0002-3228-9692
Alasdair J ColesDepartment of Clinical Neurosciences, University of Cambridge, United Kingdom.ORCID 0000-0003-4738-0760
University of Cambridge · GBAllen Institute for Brain Science · USARVYS Proteins (United States) · USKarolinska Institutet · SESahlgrenska University Hospital · SEUniversity of Gothenburg · SEKarolinska University Hospital · SEMario Negri Institute for Pharmacological Research · IT

Funding

Medical Research Council G0802251Medical Research Council MR/R005036/1Wellcome Trust 105924Wellcome Trust RG79413
6 · The paper itself

Abstract

Most of the variation in outcome following severe traumatic brain injury (TBI) remains unexplained by currently recognized prognostic factors. Neuroinflammation may account for some of this difference. We hypothesized that TBI generated variable autoantibody responses between individuals that would contribute to outcome. We developed a custom protein microarray to detect autoantibodies to both CNS and systemic Ags in serum from the acute-phase (the first 7 d), late (6-12 mo), and long-term (6-13 y) intervals after TBI in human patients. We identified two distinct patterns of immune response to TBI. The first was a broad response to the majority of Ags tested, predominantly IgM mediated in the acute phase, then IgG dominant at late and long-term time points. The second was responses to specific Ags, most frequently myelin-associated glycopeptide (MAG), which persisted for several months post-TBI but then subsequently resolved. Exploratory analyses suggested that patients with a greater acute IgM response experienced worse outcomes than predicted from current known risk factors, suggesting a direct or indirect role in worsening outcome. Furthermore, late persistence of anti-MAG IgM autoantibodies correlated with raised serum neurofilament light concentrations at these time points, suggesting an association with ongoing neurodegeneration over the first year postinjury. Our results show that autoantibody production occurs in some individuals following TBI, can persist for many years, and is associated with worse patient outcome. The complexity of responses means that conventional approaches based on measuring responses to single antigenic targets may be misleading.

Indexed as

AdultAutoantibodiesBrain Injuries, TraumaticFemaleHumansMaleMiddle AgedYoung AdultAutoantibodies

Identifiers

PMID34145056
PMCPMC7616895
OpenAlexW3168346142

What OpenQuestion holds

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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 OpenQuestion graph.