Evidence map›Paper›PMID 32499518›Full record

ArticleCell death & disease2020

TonEBP in dendritic cells mediates pro-inflammatory maturation and Th1/Th17 responses.

Byeong Jin Ye, Hwan Hee Lee, Eun Jin Yoo, Chae Young Lee, Jun Ho Lee, Hyun Je Kang, Gyu Won Jeong, Hyun Park, Whaseon Lee-Kwon, Soo Youn Choi and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

14 citing papers in PubMed, 16 citations in OpenAlex.

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  5. Lymphangiogenesis: A new strategy for heart disease treatment (Review).International journal of molecular medicine · 2024
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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

11 authors at 1 institution in 1 country.

Byeong Jin YeSchool of Life Sciences, Ulsan National Institute of Science and Technology, Ulsan, 44919, Republic of Korea.
Hwan Hee LeeSchool of Life Sciences, Ulsan National Institute of Science and Technology, Ulsan, 44919, Republic of Korea.
Eun Jin YooSchool of Life Sciences, Ulsan National Institute of Science and Technology, Ulsan, 44919, Republic of Korea.
Chae Young LeeSchool of Life Sciences, Ulsan National Institute of Science and Technology, Ulsan, 44919, Republic of Korea.
Jun Ho LeeSchool of Life Sciences, Ulsan National Institute of Science and Technology, Ulsan, 44919, Republic of Korea.
Hyun Je KangSchool of Life Sciences, Ulsan National Institute of Science and Technology, Ulsan, 44919, Republic of Korea.
Gyu Won JeongSchool of Life Sciences, Ulsan National Institute of Science and Technology, Ulsan, 44919, Republic of Korea.
Hyun ParkSchool of Life Sciences, Ulsan National Institute of Science and Technology, Ulsan, 44919, Republic of Korea.
Whaseon Lee-KwonSchool of Life Sciences, Ulsan National Institute of Science and Technology, Ulsan, 44919, Republic of Korea.
Soo Youn ChoiSchool of Life Sciences, Ulsan National Institute of Science and Technology, Ulsan, 44919, Republic of Korea. sychoi@unist.ac.kr.ORCID http://orcid.org/0000-0002-3149-5590
Hyug Moo KwonSchool of Life Sciences, Ulsan National Institute of Science and Technology, Ulsan, 44919, Republic of Korea. hmkwon@unist.ac.kr.
Ulsan National Institute of Science and Technology · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dendritic cells (DCs) are potent antigen-presenting cells that link the innate and adaptive immune responses; as such they play pivotal roles in initiation and progression of rheumatoid arthritis (RA). Here, we report that the tonicity-responsive enhancer-binding protein (TonEBP or NFAT5), a Rel family protein involved in the pathogenesis of autoimmune disease and inflammation, is required for maturation and function of DCs. Myeloid cell-specific TonEBP deletion reduces disease severity in a murine model of collagen-induced arthritis; it also inhibits maturation of DCs and differentiation of pathogenic Th1 and Th17 cells in vivo. Upon stimulation by TLR4, TonEBP promotes surface expression of major histocompatibility complex class II and co-stimulatory molecules via p38 mitogen-activated protein kinase. This is followed by DC-mediated differentiation of pro-inflammatory Th1 and Th17 cells. Taken together, these findings provide mechanistic basis for the pathogenic role of TonEBP in RA and possibly other autoimmune diseases.

Indexed as

AnimalsArthritis, ExperimentalCell DifferentiationCell ProliferationDendritic CellsDisease Models, AnimalInflammationLipopolysaccharidesLymphocyte ActivationMaleMice, Inbred C57BLModels, BiologicalMyeloid CellsNFATC Transcription Factorsp38 Mitogen-Activated Protein KinasesSeverity of Illness IndexLipopolysaccharidesNFATC Transcription Factorsp38 Mitogen-Activated Protein Kinases

Identifiers

PMID32499518
PMCPMC7272407
OpenAlexW3033893997

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.