Evidence map›Paper›PMID 36623588›Full record

ArticleMucosal immunology2023

CD200R1 promotes interleukin-17 production by group 3 innate lymphoid cells by enhancing signal transducer and activator of transcription 3 activation.

Holly Linley, Alice Ogden, Shafqat Jaigirdar, Lucy Buckingham, Joshua Cox, Megan Priestley, Amy Saunders

Open access · hybridAbstract read
In one paragraph

Article in Mucosal immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

12 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. The Immunology of Psoriasis-Current Concepts in Pathogenesis.Clinical reviews in allergy & immunology · 2024
    Review
  11. Review
  12. ILC3: a case of conflicted identity.Frontiers in immunology · 2023
    Review
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

7 authors at 1 institution in 1 country.

Holly LinleyManchester Collaborative Centre for Inflammation Research, Manchester, UK; Lydia Becker Institute of Immunology and Inflammation, Division of Infection, Immunity and Respiratory Medicine, School of Biological Science, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Academic Health Science Centre, Manchester, UK.
Alice OgdenManchester Collaborative Centre for Inflammation Research, Manchester, UK; Lydia Becker Institute of Immunology and Inflammation, Division of Infection, Immunity and Respiratory Medicine, School of Biological Science, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Academic Health Science Centre, Manchester, UK.
Shafqat JaigirdarManchester Collaborative Centre for Inflammation Research, Manchester, UK; Lydia Becker Institute of Immunology and Inflammation, Division of Infection, Immunity and Respiratory Medicine, School of Biological Science, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Academic Health Science Centre, Manchester, UK.
Lucy BuckinghamManchester Collaborative Centre for Inflammation Research, Manchester, UK; Lydia Becker Institute of Immunology and Inflammation, Division of Infection, Immunity and Respiratory Medicine, School of Biological Science, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Academic Health Science Centre, Manchester, UK.
Joshua CoxManchester Collaborative Centre for Inflammation Research, Manchester, UK; Lydia Becker Institute of Immunology and Inflammation, Division of Infection, Immunity and Respiratory Medicine, School of Biological Science, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Academic Health Science Centre, Manchester, UK.
Megan PriestleyManchester Collaborative Centre for Inflammation Research, Manchester, UK; Lydia Becker Institute of Immunology and Inflammation, Division of Infection, Immunity and Respiratory Medicine, School of Biological Science, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Academic Health Science Centre, Manchester, UK.
Amy SaundersManchester Collaborative Centre for Inflammation Research, Manchester, UK; Lydia Becker Institute of Immunology and Inflammation, Division of Infection, Immunity and Respiratory Medicine, School of Biological Science, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Academic Health Science Centre, Manchester, UK. Electronic address: amy.saunders@manchester.ac.uk.
Manchester Academic Health Science Centre · GB

Funding

Biotechnology and Biological Sciences Research CouncilWellcome Trust 109375Wellcome Trust 109375/Z/15/Z
6 · The paper itself

Abstract

Psoriasis is a common chronic inflammatory skin disease with no cure. It is driven by the interleukin (IL)-23/IL-17A axis and type 17 T helper cells; however, recently, group 3 innate lymphoid cells (ILC3s) have also been implicated. Despite being the focus of much research, factors regulating the activity of ILC3s remain incompletely understood. Immune regulatory pathways are particularly important at barrier sites, such as the skin, gut, and lungs, which are exposed to environmental substances and microbes. CD200R1 is an immune regulatory cell surface receptor that inhibits proinflammatory cytokine production in myeloid cells. CD200R1 is also highly expressed on ILCs, where its function remains largely unexplored. We previously observed reduced CD200R1 signaling in psoriasis-affected skin, suggesting that dysregulation may promote disease. Here, we show that contrary to this, psoriasis models are less severe in CD200R1-deficient mice due to reduced IL-17 production. Here, we uncover a key cell-intrinsic role for CD200R1 in promoting IL-23-driven IL-17A production by ILC3s by promoting signal transducer and activator of transcription 3 activation. Therefore, contrary to its inhibitory role in myeloid cells, CD200R1 is required on ILC3 to promote IL-23-stimulated signal transducer and activator of transcription 3 activation, triggering optimal IL-17 production.

Indexed as

Interleukin-17Orexin ReceptorsPsoriasisSTAT3 Transcription FactorAnimalsImmunity, InnateInterleukin-23LymphocytesMiceCd200r1 protein, mouseInterleukin-17Interleukin-23Orexin ReceptorsSTAT3 Transcription Factor

Identifiers

PMID36623588
PMCPMC10270648
OpenAlexW4313626963

What Socratic 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 Socratic graph.