Evidence map›Paper›PMID 29928274›Full record

ArticleFrontiers in immunology2018

Sialylated Autoantigen-Reactive IgG Antibodies Attenuate Disease Development in Autoimmune Mouse Models of Lupus Nephritis and Rheumatoid Arthritis.

Yannic C Bartsch, Johann Rahmöller, Maria M M Mertes, Susanne Eiglmeier, Felix K M Lorenz, Alexander D Stoehr, Dominique Braumann, Alexandra K Lorenz, André Winkler, Gina-Maria Lilienthal and 10 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
5.6field-weighted citation impact, top 3% 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

47 citing papers in PubMed, 73 citations in OpenAlex.

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  15. Serum immunoglobulin and the threshold of Fc receptor-mediated immune activation.Biochimica et biophysica acta. General subjects · 2023
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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

20 authors at 5 institutions in 1 country.

Yannic C BartschLaboratories of Immunology and Antibody Glycan Analysis, Institute for Nutrition Medicine, University of Lübeck and University Medical Center Schleswig-Holstein, Lübeck, Germany.
Johann RahmöllerLaboratories of Immunology and Antibody Glycan Analysis, Institute for Nutrition Medicine, University of Lübeck and University Medical Center Schleswig-Holstein, Lübeck, Germany.
Maria M M MertesLaboratory of Tolerance and Autoimmunity, German Rheumatism Research Center, An Institute of the Leibniz Association, Berlin, Germany.
Susanne EiglmeierLaboratory of Tolerance and Autoimmunity, German Rheumatism Research Center, An Institute of the Leibniz Association, Berlin, Germany.
Felix K M LorenzLaboratory of Tolerance and Autoimmunity, German Rheumatism Research Center, An Institute of the Leibniz Association, Berlin, Germany.
Alexander D StoehrLaboratory of Tolerance and Autoimmunity, German Rheumatism Research Center, An Institute of the Leibniz Association, Berlin, Germany.
Dominique BraumannLaboratories of Immunology and Antibody Glycan Analysis, Institute for Nutrition Medicine, University of Lübeck and University Medical Center Schleswig-Holstein, Lübeck, Germany.
Alexandra K LorenzLaboratory of Tolerance and Autoimmunity, German Rheumatism Research Center, An Institute of the Leibniz Association, Berlin, Germany.
André WinklerLaboratory of Tolerance and Autoimmunity, German Rheumatism Research Center, An Institute of the Leibniz Association, Berlin, Germany.
Gina-Maria LilienthalLaboratories of Immunology and Antibody Glycan Analysis, Institute for Nutrition Medicine, University of Lübeck and University Medical Center Schleswig-Holstein, Lübeck, Germany.
Janina PetryLaboratories of Immunology and Antibody Glycan Analysis, Institute for Nutrition Medicine, University of Lübeck and University Medical Center Schleswig-Holstein, Lübeck, Germany.
Juliane HobuschLaboratories of Immunology and Antibody Glycan Analysis, Institute for Nutrition Medicine, University of Lübeck and University Medical Center Schleswig-Holstein, Lübeck, Germany.
Moritz SteinhausLaboratories of Immunology and Antibody Glycan Analysis, Institute for Nutrition Medicine, University of Lübeck and University Medical Center Schleswig-Holstein, Lübeck, Germany.
Constanze HessLaboratory of Tolerance and Autoimmunity, German Rheumatism Research Center, An Institute of the Leibniz Association, Berlin, Germany.
Vivien HolecskaLaboratory of Tolerance and Autoimmunity, German Rheumatism Research Center, An Institute of the Leibniz Association, Berlin, Germany.
Carolin T SchoenLaboratory of Tolerance and Autoimmunity, German Rheumatism Research Center, An Institute of the Leibniz Association, Berlin, Germany.
Carolin M OefnerLaboratory of Tolerance and Autoimmunity, German Rheumatism Research Center, An Institute of the Leibniz Association, Berlin, Germany.
Alexei LeliavskiLaboratories of Immunology and Antibody Glycan Analysis, Institute for Nutrition Medicine, University of Lübeck and University Medical Center Schleswig-Holstein, Lübeck, Germany.
Véronique BlanchardLaboratory of Glycodesign and Glycoanalytics, Institute for Laboratory Medicine, Clinical Chemistry and Pathobiochemistry, Charité - University Medicine Berlin, Berlin, Germany.
Marc EhlersLaboratories of Immunology and Antibody Glycan Analysis, Institute for Nutrition Medicine, University of Lübeck and University Medical Center Schleswig-Holstein, Lübeck, Germany.
Leibniz Association · DEUniversity of Lübeck · DEGerman Rheumatism Research Centre · DECharité - Universitätsmedizin Berlin · DEGerman Center for Lung Research · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pro- and anti-inflammatory effector functions of IgG antibodies (Abs) depend on their subclass and Fc glycosylation pattern. Accumulation of non-galactosylated (agalactosylated; G0) IgG Abs in the serum of rheumatoid arthritis and systemic lupus erythematosus (SLE) patients reflects severity of the diseases. In contrast, sialylated IgG Abs are responsible for anti-inflammatory effects of the intravenous immunoglobulin (pooled human serum IgG from healthy donors), administered in high doses (2 g/kg) to treat autoimmune patients. However, whether low amounts of sialylated autoantigen-reactive IgG Abs can also inhibit autoimmune diseases is hardly investigated. Here, we explore whether sialylated autoantigen-reactive IgG Abs can inhibit autoimmune pathology in different mouse models. We found that sialylated IgG auto-Abs fail to induce inflammation and lupus nephritis in a B cell receptor (BCR) transgenic lupus model, but instead are associated with lower frequencies of pathogenic Th1, Th17 and B cell responses. In accordance, the transfer of small amounts of immune complexes containing sialylated IgG Abs was sufficient to attenuate the development of nephritis. We further showed that administration of sialylated collagen type II (Col II)-specific IgG Abs attenuated the disease symptoms in a model of Col II-induced arthritis and reduced pathogenic Th17 cell and autoantigen-specific IgG Ab responses. We conclude that sialylated autoantigen-specific IgG Abs may represent a promising tool for treating pathogenic T and B cell immune responses in autoimmune diseases.

Indexed as

AnimalsArthritis, ExperimentalArthritis, RheumatoidAutoantibodiesB-LymphocytesCollagen Type IIDisease Models, AnimalGlycosylationHumansImmune ToleranceLupus NephritisMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicN-Acetylneuraminic AcidAutoantibodiesCollagen Type IIFcgr2b protein, mouseN-Acetylneuraminic AcidReceptors, Antigen, B-CellReceptors, IgGautoimmunityIgG glycosylationimmunosuppressionrheumatoid arthritissialylationST6gal1systemic lupus erythematosusTh17

Identifiers

PMID29928274
PMCPMC5997785
OpenAlexW2801444946

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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.