Evidence map›Paper›PMID 26910010›Full record

ArticleeLife2016

The autophagy gene Atg16l1 differentially regulates Treg and TH2 cells to control intestinal inflammation.

Agnieszka M Kabat, Oliver J Harrison, Thomas Riffelmacher, Amin E Moghaddam, Claire F Pearson, Adam Laing, Lucie Abeler-Dörner, Simon P Forman, Richard K Grencis, Quentin Sattentau and 3 more

Open access · goldAbstract read
In one paragraph

Article in eLife, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 120 papers.

0numbers the graph read from it
0cells of the map it votes in
120citing papers in PubMed
18.8field-weighted citation impact, top 1% 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

120 citing papers in PubMed, 188 citations in OpenAlex.

  1. Review
  2. Article
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  4. Resolving the field: a role for Nod2 in T cells.Journal of immunology (Baltimore, Md. : 1950) · 2025
    Review
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  10. Article
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  13. Article
  14. Autophagic regulation of CD8Frontiers in cellular and infection microbiology · 2025
    Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. Review

60 more citing papers are in PubMed but not listed here.

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 5 institutions in 2 countries.

Agnieszka M KabatSir William Dunn School of Pathology, University of Oxford, Oxford, United Kingdom.
Oliver J HarrisonSir William Dunn School of Pathology, University of Oxford, Oxford, United Kingdom.
Thomas RiffelmacherMRC Human Immunology Unit, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, United Kingdom.
Amin E MoghaddamSir William Dunn School of Pathology, University of Oxford, Oxford, United Kingdom.
Claire F PearsonKennedy Institute of Rheumatology, University of Oxford, Oxford, United Kingdom.
Adam LaingPeter Gorer Department of Immunobiology, King's College London, London, United Kingdom.
Lucie Abeler-DörnerPeter Gorer Department of Immunobiology, King's College London, London, United Kingdom.
Simon P FormanFaculty of Life Sciences, The University of Manchester, Manchester, United Kingdom.
Richard K GrencisFaculty of Life Sciences, The University of Manchester, Manchester, United Kingdom.
Quentin SattentauSir William Dunn School of Pathology, University of Oxford, Oxford, United Kingdom.
Anna Katharina SimonMRC Human Immunology Unit, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, United Kingdom.
Johanna PottSir William Dunn School of Pathology, University of Oxford, Oxford, United Kingdom.
Kevin J MaloySir William Dunn School of Pathology, University of Oxford, Oxford, United Kingdom.ORCID http://orcid.org/0000-0001-5795-7688
University of Oxford · GBJohn Radcliffe Hospital · GBKing's College London · GBUniversity of Manchester · GBNational Institutes of Health · US

Funding

Medical Research Council G0000635Medical Research Council MR/K011898/1Wellcome Trust 097112Wellcome Trust 100156Wellcome Trust 100290Wellcome Trust 102972
6 · The paper itself

Abstract

A polymorphism in the autophagy gene Atg16l1 is associated with susceptibility to inflammatory bowel disease (IBD); however, it remains unclear how autophagy contributes to intestinal immune homeostasis. Here, we demonstrate that autophagy is essential for maintenance of balanced CD4(+) T cell responses in the intestine. Selective deletion of Atg16l1 in T cells in mice resulted in spontaneous intestinal inflammation that was characterized by aberrant type 2 responses to dietary and microbiota antigens, and by a loss of Foxp3(+) Treg cells. Specific ablation of Atg16l1 in Foxp3(+) Treg cells in mice demonstrated that autophagy directly promotes their survival and metabolic adaptation in the intestine. Moreover, we also identify an unexpected role for autophagy in directly limiting mucosal TH2 cell expansion. These findings provide new insights into the reciprocal control of distinct intestinal TH cell responses by autophagy, with important implications for understanding and treatment of chronic inflammatory disorders.

Indexed as

AnimalsAutophagy-Related ProteinsCarrier ProteinsGene DeletionInflammatory Bowel DiseasesMiceMice, KnockoutTh2 CellsT-Lymphocytes, RegulatoryAtg16l1 protein, mouseAutophagy-Related ProteinsCarrier ProteinsautophagyIBDimmunologymousemucosal immunologyT helper cells

Identifiers

PMID26910010
PMCPMC4798959
OpenAlexW2281605325

What OpenQuestion holds

Textmetadata
LicenceCC0
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.