Evidence map›Paper›PMID 27122964›Full record

ArticleMolecular vision2016

Myelin-specific Th17 cells induce severe relapsing optic neuritis with irreversible loss of retinal ganglion cells in C57BL/6 mice.

Chelsea M Larabee, Yang Hu, Shruti Desai, Constantin Georgescu, Jonathan D Wren, Robert C Axtell, Scott M Plafker

Open access · greenAbstract read
In one paragraph

Article in Molecular vision, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

16 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
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  4. Cathepsin-B inhibitor CA-074 attenuates retinopathy and optic neuritis in experimental autoimmune encephalomyelitis induced in SJL/J mice.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2023
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  12. Protective Role of Limitrin in Experimental Autoimmune Optic Neuritis.Investigative ophthalmology & visual science · 2021
    Article
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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

7 authors at 1 institution in 1 country.

Chelsea M LarabeeOklahoma Center for Neuroscience, University of Oklahoma Health Sciences Center, Oklahoma City, OK; Aging and Metabolism Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK.
Yang HuArthritis and Clinical Immunology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK.
Shruti DesaiAging and Metabolism Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK.
Constantin GeorgescuArthritis and Clinical Immunology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK.
Jonathan D WrenArthritis and Clinical Immunology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK.
Robert C AxtellArthritis and Clinical Immunology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK.
Scott M PlafkerOklahoma Center for Neuroscience, University of Oklahoma Health Sciences Center, Oklahoma City, OK; Aging and Metabolism Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK.
Oklahoma Medical Research Foundation · US

Funding

Tracking and Evaluation CoreU54GM104938 · NIGMS · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI Valerie Williams · 2013 to 2026
$68.2M
Targeted DNA Methylation and Mitochondrial Heteroplasmy CoreP30AG050911 · NIA · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI HOLLY VAN REMMEN · 2015 to 2026
$13.9M
Treatment strategies for autoimmune demyelinating optic neuritisR21EY026684 · NEI · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI PLAFKER, SCOTT M · 2016 to 2017
$472k
NEI NIH HHS R21 EY026684NIA NIH HHS P30 AG050911NIA NIH HHS P30AG050911NIGMS NIH HHS U54 GM104938
6 · The paper itself

Abstract

purposeOptic neuritis affects most patients with multiple sclerosis (MS), and current treatments are unreliable. The purpose of this study was to characterize the contribution of Th1 and Th17 cells to the development of optic neuritis.

methodsMice were passively transferred myelin-specific Th1 or Th17 cells to induce experimental autoimmune encephalomyelitis (EAE), a model of neuroautoimmunity. Visual acuity was assessed daily with optokinetic tracking, and 1, 2, and 3 weeks post-induction, optic nerves and retinas were harvested for immunohistochemical analyses.

resultsPassive transfer experimental autoimmune encephalomyelitis elicits acute episodes of asymmetric visual deficits and is exacerbated in Th17-EAE relative to Th1-EAE. The Th17-EAE optic nerves contained more inflammatory infiltrates and an increased neutrophil to macrophage ratio. Significant geographic degeneration of the retinal ganglion cells accompanied Th17-EAE but not Th1.

conclusionsTh17-induced transfer EAE recapitulates pathologies observed in MS-associated optic neuritis, namely, monocular episodes of vision loss, optic nerve inflammation, and geographic retinal ganglion cell (RGC) degeneration.

Indexed as

AnimalsApoptosisDisease Models, AnimalEncephalomyelitis, Autoimmune, ExperimentalFemaleImmunization, PassiveMacrophagesMiceMice, Inbred C57BLMultiple SclerosisMyelin SheathNeutrophilsOptic NeuritisRetinal Ganglion CellsTh17 CellsTh1 Cells

Identifiers

PMID27122964
PMCPMC4830397
OpenAlexW2339655433

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.