Evidence map›Paper›PMID 37041208›Full record

ArticleNature communications2023

A bacterial autotransporter impairs innate immune responses by targeting the transcription factor TFE3.

Atri Ta, Rafael Ricci-Azevedo, Swathy O Vasudevan, Skylar S Wright, Puja Kumari, Morena S Havira, Meera Surendran Nair, Vijay A Rathinam, Sivapriya Kailasan Vanaja

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Review
  2. Article
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

9 authors at 3 institutions in 1 country.

Atri TaDepartment of Immunology, UConn Health School of Medicine, 263 Farmington Ave, Farmington, CT, 06030, USA.
Rafael Ricci-AzevedoDepartment of Immunology, UConn Health School of Medicine, 263 Farmington Ave, Farmington, CT, 06030, USA.ORCID 0000-0002-0020-6530
Swathy O VasudevanDepartment of Immunology, UConn Health School of Medicine, 263 Farmington Ave, Farmington, CT, 06030, USA.ORCID 0000-0001-7437-8119
Skylar S WrightDepartment of Immunology, UConn Health School of Medicine, 263 Farmington Ave, Farmington, CT, 06030, USA.ORCID 0000-0002-1341-5710
Puja KumariDepartment of Immunology, UConn Health School of Medicine, 263 Farmington Ave, Farmington, CT, 06030, USA.
Morena S HaviraArvinas, Inc., 5 Science Park, New Haven, CT, 06511, USA.
Meera Surendran NairAnimal Diagnostic Laboratory, Department of Veterinary and Biomedical Sciences, Pennsylvania State University, University Park, PA, 16802, USA.
Vijay A RathinamDepartment of Immunology, UConn Health School of Medicine, 263 Farmington Ave, Farmington, CT, 06030, USA.ORCID 0000-0002-8009-3977
Sivapriya Kailasan VanajaDepartment of Immunology, UConn Health School of Medicine, 263 Farmington Ave, Farmington, CT, 06030, USA. kailasanvanaja@uchc.edu.ORCID 0000-0001-6188-2869
UConn Health · USArvinas (United States) · USPennsylvania State University · US

Funding

Cytosolic Immune Surveillance During Bacterial InfectionsR01AI119015 · NIAID · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI RATHINAM, VIJAY · 2016 to 2025
$4.0M
Bacterial modulation of noncanonical inflammasomeR01AI132850 · NIAID · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI KAILASAN VANAJA, SIVAPRIYA · 2018 to 2022
$2.0M
Bacterial modulation of noncanonical inflammasomeR56AI132850 · NIAID · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI KAILASAN VANAJA, SIVAPRIYA · 2023 to 2023
$484k
NIAID NIH HHS R01 AI119015NIAID NIH HHS R01 AI132850NIAID NIH HHS R56 AI132850
6 · The paper itself

Abstract

Type I interferons (IFNs) are consequential cytokines in antibacterial defense. Whether and how bacterial pathogens inhibit innate immune receptor-driven type I IFN expression remains mostly unknown. By screening a library of enterohemorrhagic Escherichia coli (EHEC) mutants, we uncovered EhaF, an uncharacterized protein, as an inhibitor of innate immune responses including IFNs. Further analyses identified EhaF as a secreted autotransporter-a type of bacterial secretion system with no known innate immune-modulatory function-that translocates into host cell cytosol and inhibit IFN response to EHEC. Mechanistically, EhaF interacts with and inhibits the MiT/TFE family transcription factor TFE3 resulting in impaired TANK phosphorylation and consequently, reduced IRF3 activation and type I IFN expression. Notably, EhaF-mediated innate immune suppression promotes EHEC colonization and pathogenesis in vivo. Overall, this study has uncovered a previously unknown autotransporter-based bacterial strategy that targets a specific transcription factor to subvert innate host defense.

Indexed as

Enterohemorrhagic Escherichia coliInterferon Type IBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsImmunity, InnateTranscription FactorsType V Secretion SystemsBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsInterferon Type ITranscription FactorsType V Secretion Systems

Identifiers

PMID37041208
PMCPMC10090168
OpenAlexW4364374545

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.