Evidence map›Paper›PMID 33809015›Full record

ArticleInternational journal of molecular sciences2021

Analysis of PI3K Pathway Associated Molecules Reveals Dysregulated Innate and Adaptive Functions of B Cells in Early Diffuse Cutaneous Systemic Sclerosis.

Diána Simon, Szabina Erdő-Bonyár, Judit Rapp, Péter Balogh, Tünde Minier, Gabriella Nagy, László Czirják, Tímea Berki

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.8field-weighted citation impact, top 31% 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

4 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. 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

8 authors at 1 institution in 1 country.

Diána SimonClinical Center, Department of Immunology and Biotechnology, University of Pécs Medical School, H-7624 Pécs, Hungary.
Szabina Erdő-BonyárClinical Center, Department of Immunology and Biotechnology, University of Pécs Medical School, H-7624 Pécs, Hungary.
Judit RappClinical Center, Department of Immunology and Biotechnology, University of Pécs Medical School, H-7624 Pécs, Hungary.
Péter BaloghClinical Center, Department of Immunology and Biotechnology, University of Pécs Medical School, H-7624 Pécs, Hungary.
Tünde MinierClinical Center, Department of Rheumatology and Immunology, University of Pécs Medical School, H-7632 Pécs, Hungary.
Gabriella NagyClinical Center, Department of Rheumatology and Immunology, University of Pécs Medical School, H-7632 Pécs, Hungary.
László CzirjákClinical Center, Department of Rheumatology and Immunology, University of Pécs Medical School, H-7632 Pécs, Hungary.
Tímea BerkiClinical Center, Department of Immunology and Biotechnology, University of Pécs Medical School, H-7624 Pécs, Hungary.
University of Pecs · HU

Funding

EFOP EFOP 361-16-2016-00004GINOP GINOP-232-15-2016-00050Thematic Excellence Program 2020 - Institutional Excellence Sub-programme of the Ministry for Innovation and Technology in Hungary, within the framework of the second thematic pro-gramme of the University of Pécs TKP2020University of Pécs PTE ÁOK-KA 2020/10
6 · The paper itself

Abstract

B cell activation is an early event in the development of systemic sclerosis (SSc). The classical activation of B cells downstream of the B-cell receptor (BCR) involves the phosphatidylinositol-3 kinase (PI3K) pathway that integrates the effects of multiple co-stimulatory receptors. Our analysis of PI3K pathway associated molecules in peripheral blood B cells of early diffuse cutaneous SSc (dcSSc) patients showed altered mRNA expression of Toll-like receptor (TLR) homolog CD180, TLR4, complement component 3, IL-4 receptor and secreted phosphoprotein 1 (SPP1). Parallel to this, we found elevated basal SPP1 secretion in dcSSc B cells, but, with BCR + IL-4 receptor co-stimulation, we could not induce further secretion. CD180 stimulation alone resulted in NF-κB activation in more B cells than CD180 + BCR co-stimulation both in dcSSc and healthy control (HC), but the co-engagement increased the phosphorylation of NF-κB only in dcSSc B cells. Additionally, in contrast with HC B cells, the lower basal production of IL-10 by dcSSc B cells could not be elevated with CD180 stimulation. Furthermore, activation via CD180 increased the percentage of CD86+ switched memory (CD27+IgD-) B cells in dcSSc compared to HC. Our results suggest that alternative B cell activation and CD180 dysfunction cause imbalance of regulatory mechanisms in dcSSc B cells.

Indexed as

Antigens, CDB-LymphocytesCell LineageComplement C3FemaleGene Expression RegulationHumansInterleukin-10Lymphocyte ActivationMaleMiddle AgedNF-kappa BOsteopontinPhosphatidylinositol 3-KinasesReceptors, Interleukin-4Scleroderma, DiffuseAntigens, CDCD180 protein, humanComplement C3Interleukin-10NF-kappa BOsteopontinPhosphatidylinositol 3-KinasesReceptors, Interleukin-4SPP1 protein, humanTLR4 protein, humanToll-Like Receptor 4B cellsCD180dcSScIL-10NF-κBPI3K pathwaySPP1switched memory B cellssystemic sclerosis

Identifiers

PMID33809015
PMCPMC7998899
OpenAlexW3139259222

What Socratic holds

Textmetadata
LicenceCC BY
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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 Socratic graph.