Evidence map›Paper›PMID 31266507›Full record

ArticleJournal of neuroinflammation2019

T cell-selective deletion of Oct1 protects animals from autoimmune neuroinflammation while maintaining neurotropic pathogen response.

Heejoo Kim, Laura Dickey, Colleen Stone, Jillian L Jafek, Thomas E Lane, Dean Tantin

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.4field-weighted citation impact, top 38% 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

5 citing papers in PubMed, 9 citations in OpenAlex.

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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

6 authors at 1 institution in 1 country.

Heejoo KimDepartment of Pathology, University of Utah School of Medicine, Salt Lake City, UT, 84112, USA.
Laura DickeyDepartment of Pathology, University of Utah School of Medicine, Salt Lake City, UT, 84112, USA.
Colleen StoneDepartment of Pathology, University of Utah School of Medicine, Salt Lake City, UT, 84112, USA.
Jillian L JafekDepartment of Pathology, University of Utah School of Medicine, Salt Lake City, UT, 84112, USA.
Thomas E LaneDepartment of Pathology, University of Utah School of Medicine, Salt Lake City, UT, 84112, USA. tom.lane@path.utah.edu.
Dean TantinDepartment of Pathology, University of Utah School of Medicine, Salt Lake City, UT, 84112, USA. dean.tantin@path.utah.edu.ORCID http://orcid.org/0000-0003-1354-8385
University of Utah · US

Funding

Utah Center for Clinical and Translational ScienceUL1TR002538 · NCATS · UNIVERSITY OF UTAH · PI HESS, RACHEL, MAJERSIK, JENNIFER JUHL · 2018 to 2022
$26.0M
TRAINING PROGRAM IN GENETICST32GM007464 · NIGMS · UNIVERSITY OF UTAH · PI GRUNWALD, DAVID J., STANFIELD, GILLIAN · 1985 to 2020
$6.1M
Chemokines and Viral-Induced Neurologic DiseaseR01NS041249 · NINDS · UNIVERSITY OF UTAH · PI LANE, THOMAS E · 2002 to 2019
$5.4M
Role of Transcription Coactivator OCA-B in Gene Poising and Immunological MemoryR01AI100873 · NIAID · UNIVERSITY OF UTAH · PI TANTIN, DEAN · 2013 to 2022
$3.8M
NCATS NIH HHS UL1 TR002538NIAID NIH HHS R01 AI100873NIGMS NIH HHS T32 GM007464NINDS NIH HHS R01 NS041249NINDS NIH HHS R01NS041249
6 · The paper itself

Abstract

backgroundTreatments for autoimmune diseases aim to dampen autoreactivity while preserving normal immune function. In CD4

objectiveWe used a conditional mouse Oct1 (Pou2f1) allele and a CD4-Cre driver to determine the effect of T cell-specific Oct1 loss on autoimmune- and viral-induced neuroinflammation using an autoantigen-driven EAE model of autoimmunity and a JHMV model of viral infection.

resultsOct1 conditional deletion mitigated clinical scores and reduced infiltrating T cells and cytokine production in the EAE model. Consistently, Oct1-deficient CD4

conclusionOur findings uncover a significant difference between the effect of Oct1 loss on autoimmune and anti-pathogen responses, which potentially could be exploited for therapeutic benefit.

Indexed as

Amino Acid SequenceAnimalsAutoimmunityCD4-Positive T-LymphocytesEncephalomyelitis, Autoimmune, ExperimentalInflammationInflammation MediatorsMiceMice, Inbred C57BLMice, TransgenicNerve Growth FactorsOctamer Transcription Factor-1Inflammation MediatorsNerve Growth FactorsOctamer Transcription Factor-1Pou2f1 protein, mouseExperimental autoimmune encephalomyelitisJHMVOct1/POU2F1T lymphocytes

Identifiers

PMID31266507
PMCPMC6607600
OpenAlexW2955504395

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.