Evidence map›Paper›PMID 37462681›Full record

ArticleJournal of Crohn's & colitis2023

An Intestinal Th17 Subset is Associated with Inflammation in Crohn's Disease and Activated by Adherent-invasive Escherichia coli.

Moira Paroni, Gabriella Leccese, Valeria Ranzani, Giorgia Moschetti, Matteo Chiara, Federica Perillo, Sara Ferri, Francesca Clemente, Daniele Noviello, Francesco Simone Conforti and 16 more

Open access · hybridAbstract read
In one paragraph

Article in Journal of Crohn's & colitis, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

27 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
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  4. Deciphering the Implications ofPathogens (Basel, Switzerland) · 2026
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  11. World journal of gastroenterology · 2025
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  19. Frontiers in immunology · 2025
    Article
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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

26 authors at 7 institutions in 1 country.

Moira ParoniINGM-National Institute of Molecular Genetics 'Romeo ed Enrica Invernizzi', Milan, Italy.ORCID 0000-0001-8199-3128
Gabriella LecceseDepartment of Biosciences, Università degli Studi di Milano, Milan, Italy.
Valeria RanzaniINGM-National Institute of Molecular Genetics 'Romeo ed Enrica Invernizzi', Milan, Italy.
Giorgia MoschettiINGM-National Institute of Molecular Genetics 'Romeo ed Enrica Invernizzi', Milan, Italy.ORCID 0000-0001-7763-4421
Matteo ChiaraDepartment of Biosciences, Università degli Studi di Milano, Milan, Italy.ORCID 0000-0003-3983-4961
Federica PerilloDepartment of Experimental Oncology, European Institute of Oncology, Milan, Italy.
Sara FerriDepartment of Biotechnology and Bioscience, University of Milano-Bicocca, Milan, Italy.
Francesca ClementeINGM-National Institute of Molecular Genetics 'Romeo ed Enrica Invernizzi', Milan, Italy.
Daniele NovielloGastroenterology and Endoscopy Unit, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Milan, Italy.ORCID 0000-0002-3482-0109
Francesco Simone ConfortiGastroenterology and Endoscopy Unit, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Milan, Italy.
Stefano FerreroPathology Unit, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Milan, Italy.
Bhavna KarnaniINGM-National Institute of Molecular Genetics 'Romeo ed Enrica Invernizzi', Milan, Italy.
Roberto BosottiINGM-National Institute of Molecular Genetics 'Romeo ed Enrica Invernizzi', Milan, Italy.
Chiara VascoINGM-National Institute of Molecular Genetics 'Romeo ed Enrica Invernizzi', Milan, Italy.
Serena CurtiINGM-National Institute of Molecular Genetics 'Romeo ed Enrica Invernizzi', Milan, Italy.
Maria Cristina CrostiINGM-National Institute of Molecular Genetics 'Romeo ed Enrica Invernizzi', Milan, Italy.ORCID 0000-0001-8314-1391
Paola GruarinINGM-National Institute of Molecular Genetics 'Romeo ed Enrica Invernizzi', Milan, Italy.
Grazisa RossettiINGM-National Institute of Molecular Genetics 'Romeo ed Enrica Invernizzi', Milan, Italy.
Maria Pia ConteDepartment of Public Health and Infectious Diseases, 'Sapienza' University of Rome, Rome, Italy.
Maurizio VecchiGastroenterology and Endoscopy Unit, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Milan, Italy.ORCID 0000-0003-1558-8604
Massimiliano PaganiINGM-National Institute of Molecular Genetics 'Romeo ed Enrica Invernizzi', Milan, Italy.
Paolo LandiniDepartment of Biosciences, Università degli Studi di Milano, Milan, Italy.
Federica FacciottiINGM-National Institute of Molecular Genetics 'Romeo ed Enrica Invernizzi', Milan, Italy.ORCID 0000-0002-2541-9428
Sergio AbrignaniINGM-National Institute of Molecular Genetics 'Romeo ed Enrica Invernizzi', Milan, Italy.
Flavio CaprioliGastroenterology and Endoscopy Unit, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Milan, Italy.
Jens GeginatINGM-National Institute of Molecular Genetics 'Romeo ed Enrica Invernizzi', Milan, Italy.
University of Milan · ITIstituto Nazionale Genetica Molecolare · ITEuropean Institute of Oncology · ITFondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico · ITIFOM · ITSapienza University of Rome · ITUniversity of Milano-Bicocca · IT

Funding

Italy's Ministry of Health
6 · The paper itself

Abstract

IFNγ-producing ex-Th17 cells ['Th1/17'] were shown to play a key pathogenic role in experimental colitis and are abundant in the intestine. Here, we identified and characterised a novel, potentially colitogenic subset of Th17 cells in the intestine of patients with Crohn's disease [CD]. Human Th17 cells expressing CCR5 ['pTh17'] co-expressed T-bet and RORC/γt and produced very high levels of IL-17, together with IFN-γ. They had a gene signature of Th17 effector cells and were distinct from established Th1/17 cells. pTh17 cells, but not Th1/17 cells, were associated with intestinal inflammation in CD, and decreased upon successful anti-TNF therapy with infliximab. Conventional CCR5[-]Th17 cells differentiated to pTh17 cells with IL-23 in vitro. Moreover, anti-IL-23 therapy with risankizumab strongly reduced pTh17 cells in the intestine. Importantly, intestinal pTh17 cells were selectively activated by adherent-invasive Escherichia coli [AIEC], but not by a commensal/probiotic E. coli strain. AIEC induced high levels of IL-23 and RANTES from dendritic cells [DC]. Intestinal CCR5+Th1/17 cells responded instead to cytomegalovirus and were reduced in ulcerative colitis [UC], suggesting an unexpected protective role. In conclusion, we identified an IL-23-inducible subset of human intestinal Th17 cells. pTh17 cells produced high levels of pro-inflammatory cytokines, were selectively associated with intestinal inflammation in CD, and responded to CD-associated AIEC, suggesting a key colitogenic role.

Indexed as

Crohn DiseaseEscherichia coli InfectionsBacterial AdhesionEscherichia coliHumansInflammationInterleukin-23Intestinal MucosaIntestinesTh17 CellsTumor Necrosis Factor InhibitorsInterleukin-23Tumor Necrosis Factor Inhibitors

Identifiers

PMID37462681
PMCPMC10798865
OpenAlexW4384627137

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.