Evidence map›Paper›PMID 34467524›Full record

ArticleAllergy2022

Patients with systemic sclerosis show phenotypic and functional defects in neutrophils.

Daniela Impellizzieri, Cecilie Egholm, Alan Valaperti, Oliver Distler, Onur Boyman

Open access · bronzeAbstract read
In one paragraph

Article in Allergy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

16 citing papers in PubMed, 31 citations in OpenAlex.

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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

5 authors at 2 institutions in 1 country.

Daniela ImpellizzieriDepartment of Immunology, University Hospital Zurich, Zurich, Switzerland.
Cecilie EgholmDepartment of Immunology, University Hospital Zurich, Zurich, Switzerland.
Alan ValapertiDepartment of Immunology, University Hospital Zurich, Zurich, Switzerland.
Oliver DistlerDepartment of Rheumatology, University Hospital Zurich, Zurich, Switzerland.
Onur BoymanDepartment of Immunology, University Hospital Zurich, Zurich, Switzerland.ORCID 0000-0001-8279-5545
University Hospital of Zurich · CHUniversity of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSystemic sclerosis (SSc) is a multiorgan autoimmune disease characterized by inflammation, vascular modification, and progressive fibrosis of the skin and several visceral organs. Innate and adaptive immune cells, including myeloid, B and T cells, are believed to be central to the pathogenesis of SSc. However, the role and functional state of neutrophil granulocytes (neutrophils) are ill-defined in SSc.

methodsWe performed a prospective study of neutrophils freshly isolated from SSc patients and healthy donors (HD) by measuring in these neutrophils (i) functional cell surface markers, including CD16, CD62L, CD66b, CD66c, CXCR1, CXCR2, and CXCR4; (ii) cytokine-activated intracellular signal transducer and activator of transcription (STAT) pathways, such as phosphorylated STAT3 (pSTAT3), pSTAT5, and pSTAT6; (iii) production of neutrophil extracellular traps (NET) and intracellular myeloperoxidase (MPO); and (iv) phagocytosis of bacteria by the neutrophils.

resultsNeutrophils of SSc patients expressed lower CD16 and CD62L and higher pSTAT3 and pSTAT6 compared to HD. Moreover, neutrophils of SSc patients lacked CXCR1 and CXCR2, the receptors responding to the potent neutrophil chemoattractant CXCL8. Neutrophils of SSc patients were also deficient in MPO levels, NET formation, and phagocytosis of bacteria.

conclusionsNeutrophils of patients with SSc display several functional defects affecting cell migration, NET formation, and phagocytosis of bacteria.

Indexed as

Extracellular TrapsScleroderma, SystemicHumansNeutrophilsPhagocytosisProspective StudiesIL-4 receptorinflammationinnate immunityneutrophilsystemic sclerosis

Identifiers

PMID34467524
PMCPMC9293168
OpenAlexW3196483477

What OpenQuestion holds

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LicenceCC BY-NC
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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.