Evidence map›Paper›PMID 30116249›Full record

ArticleFrontiers in immunology2018

The p.Arg435His Variation of IgG3 With High Affinity to FcRn Is Associated With Susceptibility for Pemphigus Vulgaris-Analysis of Four Different Ethnic Cohorts.

Andreas Recke, Sarah Konitzer, Susanne Lemcke, Miriam Freitag, Nele Maxi Sommer, Mohammad Abdelhady, Mahsa M Amoli, Sandrine Benoit, Farha El-Chennawy, Mohammad Eldarouti and 19 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 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

12 citing papers in PubMed, 19 citations in OpenAlex.

  1. Targeting FcRn for immunomodulation: a promising therapy in autoimmune inflammatory rheumatic diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
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  10. The pathogenesis of bullous skin diseases.Journal of translational autoimmunity · 2019
    Review
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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

29 authors at 17 institutions in 5 countries.

Andreas ReckeLübeck Institute of Experimental Dermatology (LIED), University of Lübeck, Lübeck, Germany.
Sarah KonitzerLübeck Institute of Experimental Dermatology (LIED), University of Lübeck, Lübeck, Germany.
Susanne LemckeLübeck Institute of Experimental Dermatology (LIED), University of Lübeck, Lübeck, Germany.
Miriam FreitagLübeck Institute of Experimental Dermatology (LIED), University of Lübeck, Lübeck, Germany.
Nele Maxi SommerLübeck Institute of Experimental Dermatology (LIED), University of Lübeck, Lübeck, Germany.
Mohammad AbdelhadyDepartment of Dermatology, Faculty of Medicine, Cairo University, Giza, Egypt.
Mahsa M AmoliMetabolic Disorders Research Center, Endocrinology and Metabolism Molecular - Cellular Sciences Institute, Tehran University of Medical Sciences, Tehran, Iran.
Sandrine BenoitDepartment of Dermatology, Venereology and Allergology, University Hospital Würzburg, Würzburg, Germany.
Farha El-ChennawyDepartment of Clinical Pathology, Mansoura Faculty of Medicine, Mansoura University, Mansoura, Egypt.
Mohammad EldaroutiDepartment of Dermatology, Faculty of Medicine, Cairo University, Giza, Egypt.
Rüdiger EmingDepartment of Dermatology and Allergology, Phillips-Universität Marburg, Marburg, Germany.
Regine GläserDepartment of Dermatology, Venereology and Allergology, Christian Albrecht University, Kiel, Germany.
Claudia GüntherDepartment of Dermatology, University Hospital of Dresden, Dresden, Germany.
Eva HadaschikDepartment of Dermatology, Ruprecht-Karls-University of Heidelberg, Heidelberg, Germany.
Bernhard HomeyDepartment of Dermatology, Heinrich Heine University, Düsseldorf, Germany.
Wolfgang LiebInstitute of Epidemiology, Christian-Albrechts-University, Kiel, Germany.
Wiebke K PeitschDepartment of Dermatology, University Medical Center Mannheim, Heidelberg University, Mannheim, Germany.
Claudia PföhlerDepartment of Dermatology, Saarland University Medical School, Homburg/Saar, Germany.
Reza M RobatiSkin Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Marjan SaeediSkin Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Miklós SárdyDepartment of Dermatology, Ludwig Maximilian University Munich, Munich, Germany.
Michael SticherlingDepartment of Dermatology, University of Erlangen-Nuremberg, Erlangen, Germany.
Soner UzunDepartment of Dermatology, Faculty of Medicine, Akdeniz University, Antalya, Turkey.
Margitta WormDepartment of Dermatology, Venerology and Allergology, Allergy Center Charité, Charité-Medical University Berlin, Berlin, Germany.
Detlef ZillikensDepartment of Dermatology, Allergology and Venereology, University of Lübeck, Lübeck, Germany.
Saleh IbrahimLübeck Institute of Experimental Dermatology (LIED), University of Lübeck, Lübeck, Germany.
Gestur VidarssonDepartment of Experimental Hematology, Sanquin Research Institute, Amsterdam, Netherlands.
Enno SchmidtLübeck Institute of Experimental Dermatology (LIED), University of Lübeck, Lübeck, Germany.
German AIBD Genetic Study Group
University of Lübeck · DECairo University · EGKiel University · DEShahid Beheshti University of Medical Sciences · IRAkdeniz University · TRCharité - Universitätsmedizin Berlin · DEFriedrich-Alexander-Universität Erlangen-Nürnberg · DEHeidelberg University · DEHeinrich Heine University Düsseldorf · DELudwig-Maximilians-Universität München · DEMansoura University · EGPhilipps University of Marburg · DESaarland University · DESanquin · NLTehran University of Medical Sciences · IRUniversitätsklinikum Würzburg · DEUniversity Hospital Heidelberg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

IgG3 is the IgG subclass with the strongest effector functions among all four IgG subclasses and the highest degree of allelic variability among all constant immunoglobulin genes. Due to its genetic position, IgG3 is often the first isotype an antibody switches to before IgG1 or IgG4. Compared with the other IgG subclasses, it has a reduced half-life which is probably connected to a decreased affinity to the neonatal Fc receptor (FcRn). However, a few allelic variants harbor an amino acid replacement of His435 to Arg that reverts the half-life of the resulting IgG3 to the same level as the other IgG subclasses. Because of its functional impact, we hypothesized that the p.Arg435His variation could be associated with susceptibility to autoantibody-mediated diseases like pemphigus vulgaris (PV) and bullous pemphigoid (BP). Using a set of samples from German, Turkish, Egyptian, and Iranian patients and controls, we were able to demonstrate a genetic association of the p.Arg435His variation with PV risk, but not with BP risk. Our results suggest a hitherto unknown role for the function of IgG3 in the pathogenesis of PV.

Indexed as

Genetic Predisposition to DiseaseAllelesAnalysis of VarianceCohort StudiesEgyptEnzyme-Linked Immunosorbent AssayEthnicityGenetic VariationGenome, HumanGenotypeGenotyping TechniquesGermanyHistocompatibility Antigens Class IHumansImmunoglobulin GIranFc receptor, neonatalHistocompatibility Antigens Class IImmunoglobulin GReceptors, Fcallotypeautoantibodiesdermatologyfunctional geneticshalf-lifeimmunologypemphigoidpemphigus

Identifiers

PMID30116249
PMCPMC6082936
OpenAlexW2890822497

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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.