Evidence map›Paper›PMID 28696309›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2017

Influenza infection triggers disease in a genetic model of experimental autoimmune encephalomyelitis.

Stephen Blackmore, Jessica Hernandez, Michal Juda, Emily Ryder, Gregory G Freund, Rodney W Johnson, Andrew J Steelman

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

30 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
  2. β-oxidation-mediated differentiation of effector CD4Journal of neuroinflammation · 2026
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  20. Astrocytes lure CXCR2-expressing CD4Proceedings of the National Academy of Sciences of the United States of America · 2021
    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

7 authors at 1 institution in 1 country.

Stephen BlackmoreDepartment of Animal Sciences, University of Illinois Urbana-Champaign, Urbana, IL 61801.
Jessica HernandezDepartment of Animal Sciences, University of Illinois Urbana-Champaign, Urbana, IL 61801.
Michal JudaDepartment of Animal Sciences, University of Illinois Urbana-Champaign, Urbana, IL 61801.
Emily RyderNeuroscience Program, University of Illinois Urbana-Champaign, Urbana, IL 61801.
Gregory G FreundDepartment of Animal Sciences, University of Illinois Urbana-Champaign, Urbana, IL 61801.
Rodney W JohnsonDepartment of Animal Sciences, University of Illinois Urbana-Champaign, Urbana, IL 61801.
Andrew J SteelmanDepartment of Animal Sciences, University of Illinois Urbana-Champaign, Urbana, IL 61801; asteelma@illinois.edu.ORCID 0000-0001-5408-0534
University of Illinois Urbana-Champaign · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple sclerosis (MS) is an autoimmune disease of the central nervous system. Most MS patients experience periods of symptom exacerbation (relapses) followed by periods of partial recovery (remission). Interestingly, upper-respiratory viral infections increase the risk for relapse. Here, we used an autoimmune-prone T-cell receptor transgenic mouse (2D2) and a mouse-adapted human influenza virus to test the hypothesis that upper-respiratory viral infection can cause glial activation, promote immune cell trafficking to the CNS, and trigger disease. Specifically, we inoculated 2D2 mice with influenza A virus (Puerto Rico/8/34; PR8) and then monitored them for symptoms of inflammatory demyelination. Clinical and histological experimental autoimmune encephalomyelitis was observed in ∼29% of infected 2D2 mice. To further understand how peripheral infection could contribute to disease onset, we inoculated wild-type C57BL/6 mice and measured transcriptomic alterations occurring in the cerebellum and spinal cord and monitored immune cell surveillance of the CNS by flow cytometry. Infection caused temporal alterations in the transcriptome of both the cerebellum and spinal cord that was consistent with glial activation and increased T-cell, monocyte, and neutrophil trafficking to the brain at day 8 post infection. Finally,

Indexed as

AlphainfluenzavirusAnimalsCerebellumChemokine CXCL5Encephalomyelitis, Autoimmune, ExperimentalImmunologic SurveillanceMiceMice, Inbred C57BLMice, TransgenicOrthomyxoviridae InfectionsSpinal CordTranscriptomeChemokine CXCL5experimental autoimmune encephalomyelitisimmune cell surveillancemultiple sclerosisneuroinflammationupper-respiratory viral infection

Identifiers

PMID28696309
PMCPMC5544260
OpenAlexW2735624552

What OpenQuestion 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 OpenQuestion graph.