Evidence map›Paper›PMID 35511484›Full record

ArticleNucleic acids research2022

A systematic comparison of FOSL1, FOSL2 and BATF-mediated transcriptional regulation during early human Th17 differentiation.

Ankitha Shetty, Subhash Kumar Tripathi, Sini Junttila, Tanja Buchacher, Rahul Biradar, Santosh D Bhosale, Tapio Envall, Asta Laiho, Robert Moulder, Omid Rasool and 3 more

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
7.0field-weighted citation impact, top 2% 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

22 citing papers in PubMed, 40 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

13 authors at 2 institutions in 3 countries.

Ankitha ShettyTurku Bioscience Centre, University of Turku and Åbo Akademi University, Turku 20520, Finland.ORCID 0000-0002-6940-2580
Subhash Kumar TripathiTurku Bioscience Centre, University of Turku and Åbo Akademi University, Turku 20520, Finland.
Sini JunttilaTurku Bioscience Centre, University of Turku and Åbo Akademi University, Turku 20520, Finland.ORCID 0000-0003-3754-5584
Tanja BuchacherTurku Bioscience Centre, University of Turku and Åbo Akademi University, Turku 20520, Finland.
Rahul BiradarTurku Bioscience Centre, University of Turku and Åbo Akademi University, Turku 20520, Finland.
Santosh D BhosaleTurku Bioscience Centre, University of Turku and Åbo Akademi University, Turku 20520, Finland.
Tapio EnvallTurku Bioscience Centre, University of Turku and Åbo Akademi University, Turku 20520, Finland.
Asta LaihoTurku Bioscience Centre, University of Turku and Åbo Akademi University, Turku 20520, Finland.
Robert MoulderTurku Bioscience Centre, University of Turku and Åbo Akademi University, Turku 20520, Finland.
Omid RasoolTurku Bioscience Centre, University of Turku and Åbo Akademi University, Turku 20520, Finland.
Sanjeev GalandeCentre of Excellence in Epigenetics, Department of Biology, Indian Institute of Science Education and Research (IISER), Pune 411008, India.
Laura L EloTurku Bioscience Centre, University of Turku and Åbo Akademi University, Turku 20520, Finland.
Riitta LahesmaaTurku Bioscience Centre, University of Turku and Åbo Akademi University, Turku 20520, Finland.
Åbo Akademi University · FIIndian Institute of Science Education and Research Pune · IN

Funding

European Research Council 677943
6 · The paper itself

Abstract

Th17 cells are essential for protection against extracellular pathogens, but their aberrant activity can cause autoimmunity. Molecular mechanisms that dictate Th17 cell-differentiation have been extensively studied using mouse models. However, species-specific differences underscore the need to validate these findings in human. Here, we characterized the human-specific roles of three AP-1 transcription factors, FOSL1, FOSL2 and BATF, during early stages of Th17 differentiation. Our results demonstrate that FOSL1 and FOSL2 co-repress Th17 fate-specification, whereas BATF promotes the Th17 lineage. Strikingly, FOSL1 was found to play different roles in human and mouse. Genome-wide binding analysis indicated that FOSL1, FOSL2 and BATF share occupancy over regulatory regions of genes involved in Th17 lineage commitment. These AP-1 factors also share their protein interacting partners, which suggests mechanisms for their functional interplay. Our study further reveals that the genomic binding sites of FOSL1, FOSL2 and BATF harbour hundreds of autoimmune disease-linked SNPs. We show that many of these SNPs alter the ability of these transcription factors to bind DNA. Our findings thus provide critical insights into AP-1-mediated regulation of human Th17-fate and associated pathologies.

Indexed as

Basic-Leucine Zipper Transcription FactorsFos-Related Antigen-2Th17 CellsTranscription Factor AP-1AnimalsCell DifferentiationFos-Related Antigen 1Gene Expression RegulationHumansMiceProto-Oncogene Proteins c-fosBasic-Leucine Zipper Transcription FactorsBATF protein, humanBatf protein, mouseFOSL2 protein, humanFos-Related Antigen 1Fos-Related Antigen-2Proto-Oncogene Proteins c-fosTranscription Factor AP-1

Identifiers

PMID35511484
PMCPMC9122603
OpenAlexW4225852092

What OpenQuestion holds

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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.