Evidence map›Paper›PMID 23653115›Full record

ArticleMucosal immunology2014

Interleukin-22 binding protein (IL-22BP) is constitutively expressed by a subset of conventional dendritic cells and is strongly induced by retinoic acid.

J C J Martin, G Bériou, M Heslan, C Chauvin, L Utriainen, A Aumeunier, C L Scott, A Mowat, V Cerovic, S A Houston and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in Mucosal immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed
6.8field-weighted citation impact, top 3% 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

83 citing papers in PubMed, 147 citations in OpenAlex.

  1. Trial
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  4. Article
  5. Alterations in mucosa branchedGut microbes · 2025
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  6. Review
  7. Article
  8. The role of IL-22 in cancer.Medical oncology (Northwood, London, England) · 2024
    Review
  9. The role of Interleukin-22 in severe acute pancreatitis.Molecular medicine (Cambridge, Mass.) · 2024
    Review
  10. Deficiency of IL-22-binding protein enhances the ability of the gut microbiota to protect against enteric pathogens.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. CD4 T-Cell Subsets and the Pathophysiology of Inflammatory Bowel Disease.International journal of molecular sciences · 2023
    Review
  17. Article
  18. Review
  19. Role of IL-22 in homeostasis and diseases of the skin.APMIS : acta pathologica, microbiologica, et immunologica Scandinavica · 2022
    Review
  20. Review

23 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

16 authors at 5 institutions in 3 countries.

J C J Martin1] INSERM Center of Research in Transplantation and Immunology, UMR1064, Nantes, France [2] CHU Nantes, Institut de Transplantation Urologie Néphrologie (ITUN), Nantes, France [3] CHU Nantes, Laboratoire d'immunologie, Nantes, France [4] Faculté de Médecine, Université de Nantes, Nantes, France.
G Bériou1] INSERM Center of Research in Transplantation and Immunology, UMR1064, Nantes, France [2] CHU Nantes, Institut de Transplantation Urologie Néphrologie (ITUN), Nantes, France.
M Heslan1] INSERM Center of Research in Transplantation and Immunology, UMR1064, Nantes, France [2] CHU Nantes, Institut de Transplantation Urologie Néphrologie (ITUN), Nantes, France.
C Chauvin1] INSERM Center of Research in Transplantation and Immunology, UMR1064, Nantes, France [2] CHU Nantes, Institut de Transplantation Urologie Néphrologie (ITUN), Nantes, France.
L UtriainenCentre for Immunobiology, Institute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, UK.
A AumeunierCentre for Immunobiology, Institute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, UK.
C L ScottCentre for Immunobiology, Institute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, UK.
A MowatCentre for Immunobiology, Institute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, UK.
V CerovicCentre for Immunobiology, Institute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, UK.
S A HoustonCentre for Immunobiology, Institute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, UK.
M LeboeufDepartment of Gene and Cell medicine and the Department of Medicine, Mount Sinai School of Medicine, New York, New York, USA.
F X Hubert1] INSERM Center of Research in Transplantation and Immunology, UMR1064, Nantes, France [2] CHU Nantes, Institut de Transplantation Urologie Néphrologie (ITUN), Nantes, France [3] Faculté de Médecine, Université de Nantes, Nantes, France.
C Hémont1] INSERM Center of Research in Transplantation and Immunology, UMR1064, Nantes, France [2] CHU Nantes, Institut de Transplantation Urologie Néphrologie (ITUN), Nantes, France [3] CHU Nantes, Laboratoire d'immunologie, Nantes, France [4] Faculté de Médecine, Université de Nantes, Nantes, France.
M MeradDepartment of Gene and Cell medicine and the Department of Medicine, Mount Sinai School of Medicine, New York, New York, USA.
S MillingCentre for Immunobiology, Institute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, UK.
R Josien1] INSERM Center of Research in Transplantation and Immunology, UMR1064, Nantes, France [2] CHU Nantes, Institut de Transplantation Urologie Néphrologie (ITUN), Nantes, France [3] CHU Nantes, Laboratoire d'immunologie, Nantes, France [4] Faculté de Médecine, Université de Nantes, Nantes, France.
University of Glasgow · GBInstitut de Transplantation Urologie en Nephrologie · FRIcahn School of Medicine at Mount Sinai · USNantes Université · FRInserm · FR

Funding

Role of Mucosal DC Subsets in the Control of Influenza A Virus ImmunityU01AI095611 · NIAID · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI MERAD, MIRIAM, PALUCKA, ANNA KAROLINA · 2011 to 2015
$1.8M
NIAID NIH HHS U01 AI095611
6 · The paper itself

Abstract

Interleukin-22 (IL-22) is mainly produced at barrier surfaces by T cells and innate lymphoid cells and is crucial to maintain epithelial integrity. However, dysregulated IL-22 action leads to deleterious inflammation and is involved in diseases such as psoriasis, intestinal inflammation, and cancer. IL-22 binding protein (IL-22BP) is a soluble inhibitory IL-22 receptor and may represent a crucial regulator of IL-22. We show both in rats and mice that, in the steady state, the main source of IL-22BP is constituted by a subset of conventional dendritic cells (DCs) in lymphoid and non-lymphoid tissues. In mouse intestine, IL-22BP was specifically expressed in lamina propria CD103(+)CD11b(+) DC. In humans, IL-22BP was expressed in immature monocyte-derived DC and strongly induced by retinoic acid but dramatically reduced upon maturation. Our data suggest that a subset of immature DCs may actively participate in the regulation of IL-22 activity in the gut by producing high levels of IL-22BP.

Indexed as

AnimalsCD4 AntigensCell DifferentiationDendritic CellsGene Expression ProfilingGene Expression RegulationHumansIntestinal MucosaIntestinesMaleMonocytesOrgan SpecificityProtein IsoformsRatsReceptors, InterleukinSpleenCD4 Antigensinterleukin-22 receptorProtein IsoformsReceptors, InterleukinTretinoin

Identifiers

PMID23653115
PMCPMC4291114
OpenAlexW2008751364

What OpenQuestion holds

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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.