Evidence map›Paper›PMID 35759230›Full record

ArticleImmunity, inflammation and disease2022

Reduced cutaneous CD200:CD200R1 signaling in psoriasis enhances neutrophil recruitment to skin.

Holly Linley, Shafqat Jaigirdar, Karishma Mohamed, Christopher E M Griffiths, Amy Saunders

Open access · goldAbstract read
In one paragraph

Article in Immunity, inflammation and disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.4field-weighted citation impact, top 40% 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

5 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Article
  3. Serum LL-37 and inflammatory cytokines levels in psoriasis.Immunity, inflammation and disease · 2023
    Article
  4. Article
  5. 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

5 authors at 2 institutions in 1 country.

Holly LinleyManchester Collaborative Centre for Inflammation Research, Manchester, UK.
Shafqat JaigirdarManchester Collaborative Centre for Inflammation Research, Manchester, UK.
Karishma MohamedManchester Collaborative Centre for Inflammation Research, Manchester, UK.
Christopher E M GriffithsSchool of Biological Science, Manchester Academic Health Science Centre, Division of Infection and Respiratory Medicine, Lydia Becker Institute of Immunology and Inflammation, >aculty of Biology, Medicine and Health, University of Manchester, Manchester, UK.
Amy SaundersManchester Collaborative Centre for Inflammation Research, Manchester, UK.ORCID 0000-0002-2693-6435
Manchester Academic Health Science Centre · GBNational Health Service · GB

Funding

Wellcome TrustWellcome Trust 109375/Z/15/Z
6 · The paper itself

Abstract

introductionThe skin immune system is tightly regulated to prevent inappropriate inflammation in response to harmless environmental substances. This regulation is actively maintained by mechanisms including cytokines and cell surface receptors and its loss results in inflammatory disease. In the case of psoriasis, inappropriate immune activation leads to IL-17-driven chronic inflammation, but molecular mechanisms underlying this loss of regulation are not well understood. Immunoglobulin family member CD200 and its receptor, CD200R1, are important regulators of inflammation. Therefore, we determined if this pathway is dysregulated in psoriasis, and how this affects immune cell activity.

methodsHuman skin biopsies were examined by quantitative polymerase chain reaction, flow cytometry, and immunohistochemistry. The role of CD200R1 in regulating psoriasis-like skin inflammation was examined using CD200R1 blocking antibodies in mouse psoriasis models. CD200R1 blocking antibodies were also used in an in vivo neutrophil recruitment assay and in vitro assays to examine macrophage, innate lymphoid cell, γδ T cell, and neutrophil activity.

resultsWe reveal that CD200 and signaling via CD200R1 are reduced in non-lesional psoriasis skin. In mouse models of psoriasis CD200R1 was shown to limit psoriasis-like inflammation by enhancing acanthosis, CCL20 production and neutrophil recruitment, but surprisingly, macrophage function and IL-17 production were not affected, and neutrophil reactive oxygen species production was reduced.

conclusionCollectively, these data show that CD200R1 affects neutrophil function and limits inflammatory responses in healthy skin by restricting neutrophil recruitment. However, the CD200 pathway is reduced in psoriasis, resulting in a loss of immune control, and increased neutrophil recruitment in mouse models. In conclusion, we highlight CD200R1:CD200 as a pathway that might be targeted to dampen inflammation in patients with psoriasis.

Indexed as

Interleukin-17PsoriasisAnimalsAntibodies, BlockingAntigens, CDHumansImmunity, InnateInflammationLymphocytesMiceNeutrophil InfiltrationOrexin ReceptorsAntibodies, BlockingAntigens, CDantigens, CD200Cd200r1 protein, mouseInterleukin-17Orexin Receptorsinflammationneutrophilspsoriasisskin

Identifiers

PMID35759230
PMCPMC9168552
OpenAlexW4281638827

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.