Evidence map›Paper›PMID 34275478›Full record

ArticleJournal of neuroinflammation2021

Interleukin-10 deficiency exacerbates inflammation-induced tau pathology.

Lea L Weston, Shanya Jiang, Devon Chisholm, Lauren L Jantzie, Kiran Bhaskar

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 2 pooled it
5.0field-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

46 citing papers in PubMed, 2 syntheses or guidelines pooled it, 69 citations in OpenAlex.

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  20. Brain interleukins and Alzheimer's disease.Metabolic brain disease · 2025
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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

5 authors at 2 institutions in 1 country.

Lea L WestonDepartment of Molecular Genetics and Microbiology, University of New Mexico, MSC08 4660, 1 University of New Mexico, Albuquerque, NM, 87131, USA.
Shanya JiangDepartment of Molecular Genetics and Microbiology, University of New Mexico, MSC08 4660, 1 University of New Mexico, Albuquerque, NM, 87131, USA.
Devon ChisholmDepartment of Molecular Genetics and Microbiology, University of New Mexico, MSC08 4660, 1 University of New Mexico, Albuquerque, NM, 87131, USA.
Lauren L JantzieDepartment of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD, 21287, USA.
Kiran BhaskarDepartment of Molecular Genetics and Microbiology, University of New Mexico, MSC08 4660, 1 University of New Mexico, Albuquerque, NM, 87131, USA. KBhaskar@salud.unm.edu.ORCID http://orcid.org/0000-0001-6064-8106
University of New Mexico · USJohns Hopkins University · US

Funding

Unfolded Protein Response and Autophagy in T Helper Cell Effector FunctionP20GM121176 · NIGMS · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI Samuel Joseph Endicott · 2017 to 2026
$24.9M
Biology of Infectious Diseases &InflammationT32AI007538 · NIAID · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI Michelle A Ozbun · 1998 to 2026
$5.2M
Scientific CoreP20AG068077 · NIA · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI BHASKAR, KIRAN · 2020 to 2022
$3.1M
The Role of Inflammasome Signaling in TauopathiesRF1NS083704 · NINDS · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI BHASKAR, KIRAN · 2020 to 2020
$2.7M
The role of inflammasome signaling in tauopathiesR01NS083704 · NINDS · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI BHASKAR, KIRAN · 2014 to 2018
$1.4M
NIAID NIH HHS T32 AI007538NIA NIH HHS P20 AG068077NIA NIH HHS P20AG068077NIGMS NIH HHS P20 GM121176NIGMS NIH HHS P20GM121176NINDS NIH HHS R01 NS083704NINDS NIH HHS R01NS083704NINDS NIH HHS RF1 NS083704NINDS NIH HHS RF1NS083704
6 · The paper itself

Abstract

backgroundThe presence of hyperphosphorylated microtubule-associated protein tau is strongly correlated with cognitive decline and neuroinflammation in Alzheimer's disease and related tauopathies. However, the role of inflammation and anti-inflammatory interventions in tauopathies is unclear. Our goal was to determine if removing anti-inflammatory interleukin-10 (IL-10) during an acute inflammatory challenge has any effect on neuronal tau pathology.

methodsWe induce systemic inflammation in Il10-deficient (Il10

resultsOur findings show that genetic deletion of Il10 promotes enhanced neuroinflammation and tau phosphorylation. First, LPS-induced tau hyperphosphorylation was significantly increased in Il10

conclusionsThese data support that loss of IL-10 activates microglia, enhances IL-6, and leads to hyperphosphorylation of tau on AD-relevant epitopes in response to acute systemic inflammation.

Indexed as

AnimalsCell Culture TechniquesCytokinesDisease Models, AnimalImmunohistochemistryInflammationInterleukin-10Interleukin-6LipopolysaccharidesMiceMice, Inbred C57BLMice, TransgenicMicrogliaNeuronsPhosphorylationTauopathiesCytokinesInterleukin-10Interleukin-6Lipopolysaccharidestau ProteinsAlzheimer’s diseaseInterleukin-10MicrogliaNeuroinflammationTau

Identifiers

PMID34275478
PMCPMC8286621
OpenAlexW3184667630

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.