Evidence map›Paper›PMID 33912575›Full record

ArticleFrontiers in medicine2021

Neutrophil Extracellular Traps in Systemic Lupus Erythematosus Stimulate IgG2 Production From B Lymphocytes.

Roberta Bertelli, Francesca Schena, Francesca Antonini, Daniele Reverberi, Sara Signa, Nicoletta Pedemonte, Alessandro Consolaro, Marco Gattorno, Simone Negrini, Francesca Pupo and 2 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.0field-weighted citation impact, top 27% 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

11 citing papers in PubMed, 17 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

12 authors at 4 institutions in 1 country.

Roberta BertelliLaboratory of Molecular Nephrology, Division of Nephrology and Transplantation, Scientific Institute for Research, Hospitalization and Health Care (IRCCS) Giannina Gaslini Institute, Genoa, Italy.
Francesca SchenaCentre for Autoinflammatory Diseases and Immunodeficiencies, Scientific Institute for Research, Hospitalization and Health Care (IRCCS) Giannina Gaslini Institute, Genoa, Italy.
Francesca AntoniniCore Facilities Flow Cytometry and Cell Imaging Lab, Scientific Institute for Research, Hospitalization and Health Care (IRCCS) Giannina Gaslini Institute, Genoa, Italy.
Daniele ReverberiMolecular Pathology Unit, Ospedale Policlinico San Martino, Genoa, Italy.
Sara SignaCentre for Autoinflammatory Diseases and Immunodeficiencies, Scientific Institute for Research, Hospitalization and Health Care (IRCCS) Giannina Gaslini Institute, Genoa, Italy.
Nicoletta PedemonteComplex Operative Unit (UOC) of Medical Genetics, Scientific Institute for Research, Hospitalization and Health Care (IRCCS) Giannina Gaslini Institute, Genoa, Italy.
Alessandro ConsolaroPediatric Rheumatology Clinic, Scientific Institute for Research, Hospitalization and Health Care (IRCCS) Giannina Gaslini Institute, Genoa, Italy.
Marco GattornoCentre for Autoinflammatory Diseases and Immunodeficiencies, Scientific Institute for Research, Hospitalization and Health Care (IRCCS) Giannina Gaslini Institute, Genoa, Italy.
Simone NegriniDepartment of Internal Medicine, Clinical Immunology and Translational Medicine Unit, Policlinico San Martino, University of Genoa, Genoa, Italy.
Francesca PupoDepartment of Internal Medicine, Clinical Immunology and Translational Medicine Unit, Policlinico San Martino, University of Genoa, Genoa, Italy.
Stefano VolpiCentre for Autoinflammatory Diseases and Immunodeficiencies, Scientific Institute for Research, Hospitalization and Health Care (IRCCS) Giannina Gaslini Institute, Genoa, Italy.
Gian Marco GhiggeriLaboratory of Molecular Nephrology, Division of Nephrology and Transplantation, Scientific Institute for Research, Hospitalization and Health Care (IRCCS) Giannina Gaslini Institute, Genoa, Italy.
Istituto Giannina Gaslini · ITUniversity of Genoa · ITIstituti di Ricovero e Cura a Carattere Scientifico · ITOspedale Policlinico San Martino · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Circulating autoantibodies of IgG2 isotype predominate in Systemic Lupus Erythematosus (SLE) and concur to the development of the renal lesions characteristic of Lupus Nephritis (LN). Anti-dsDNA and anti-histones IgG2, together with anti-podocyte proteins (i.e., α-enolase) are the major autoantibodies in serum and renal glomeruli of LN patients. The mechanisms underlying autoantibody formation and isotype switching in SLE and LN are unknown. A major issue is how DNA/histones are externalized from cell nucleus, driving the autoimmune response. Neutrophil Extracellular Traps (NETs) have been recently identified as crucial players in this context, representing the main source of DNA and nucleosome proteins. A second key point is what regulates IgG2 isotype switching: in mouse models, T-bet transcription factor has been described as essential for IgG2a class switch. We hypothesized that, in SLE, NET formation is the key mechanism responsible for externalization of autoantigens (i.e., dsDNA, histones 2,3, and α-enolase) and that T-bet is upregulated by NETs, driving, in this way, immunoglobulin class switch recombination (CSR), with production of IgG2 autoantibodies. The data here presented show that NETs, purified from SLE patients, stimulate

Indexed as

autoimmunityIgG2lupus nephritisnaïve B cellsNETosisT-bet

Identifiers

PMID33912575
PMCPMC8072216
OpenAlexW3154969994

What OpenQuestion holds

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Registered trials

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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.