Evidence map›Paper›PMID 34348977›Full record

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

Activation of Transcription Factor 4 in Dendritic Cells Controls Th1/Th17 Responses and Autoimmune Neuroinflammation.

Indumathi Manoharan, Daniel Swafford, Arulkumaran Shanmugam, Nikhil Patel, Puttur D Prasad, Muthusamy Thangaraju, Santhakumar Manicassamy

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 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

11 citing papers in PubMed, 14 citations in OpenAlex.

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  10. A novelDiscovery immunology · 2023
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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.

Indumathi ManoharanDepartment of Biochemistry and Molecular Biology, Medical College of Georgia, Augusta University, Augusta, GA.
Daniel SwaffordGeorgia Cancer Center, Medical College of Georgia, Augusta University, Augusta, GA.
Arulkumaran ShanmugamGeorgia Cancer Center, Medical College of Georgia, Augusta University, Augusta, GA.
Nikhil PatelDepartment of Pathology, Medical College of Georgia, Augusta University, Augusta, GA; and.ORCID 0000-0001-9335-0082
Puttur D PrasadDepartment of Biochemistry and Molecular Biology, Medical College of Georgia, Augusta University, Augusta, GA.ORCID 0000-0002-8455-0186
Muthusamy ThangarajuDepartment of Biochemistry and Molecular Biology, Medical College of Georgia, Augusta University, Augusta, GA.
Santhakumar ManicassamyDepartment of Biochemistry and Molecular Biology, Medical College of Georgia, Augusta University, Augusta, GA; smanicassamy@augusta.edu.ORCID 0000-0002-2203-3917
Augusta University · US

Funding

Regulation of Oral Tolerance and Intestinal Inflammation by Beta-catenin/TCF PathR01DK097271 · NIDDK · AUGUSTA UNIVERSITY · PI MANICASSAMY, SANTHAKUMAR · 2012 to 2016
$1.6M
Regulation of colitis associated with acute kidney injury by the Wnt pathwayR01DK123360 · NIDDK · AUGUSTA UNIVERSITY · PI MANICASSAMY, SANTHAKUMAR · 2020 to 2023
$1.4M
Regulation of acute kidney injury to Candida albicans by b-catenin/TCF pathwayR21AI156103 · NIAID · AUGUSTA UNIVERSITY · PI MANICASSAMY, SANTHAKUMAR · 2021 to 2022
$424k
NIAID NIH HHS R21 AI156103NIDDK NIH HHS R01 DK097271NIDDK NIH HHS R01 DK123360
6 · The paper itself

Abstract

Dendritic cells (DCs) are professional APCs that play a crucial role in initiating robust immune responses against invading pathogens while inducing regulatory responses to the body's tissues and commensal microorganisms. A breakdown of DC-mediated immunological tolerance leads to chronic inflammation and autoimmune disorders. However, cell-intrinsic molecular regulators that are critical for programming DCs to a regulatory state rather than to an inflammatory state are not known. In this study, we show that the activation of the TCF4 transcription factor in DCs is critical for controlling the magnitude of inflammatory responses and limiting neuroinflammation. DC-specific deletion of TCF4 in mice increased Th1/Th17 responses and exacerbated experimental autoimmune encephalomyelitis pathology. Mechanistically, loss of TCF4 in DCs led to heightened activation of p38 MAPK and increased levels of proinflammatory cytokines IL-6, IL-23, IL-1β, TNF-α, and IL-12p40. Consistent with these findings, pharmacological blocking of p38 MAPK activation delayed experimental autoimmune encephalomyelitis onset and diminished CNS pathology in TCF4

Indexed as

Encephalomyelitis, Autoimmune, ExperimentalTh1 CellsAnimalsDendritic CellsMiceMice, Inbred C57BLTh17 CellsTranscription Factor 4Transcription Factor 4

Identifiers

PMID34348977
PMCPMC8415100
OpenAlexW3190620895

What OpenQuestion holds

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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.