Evidence map›Paper›PMID 32182948›Full record

ArticleCells2020

Dysregulated Antibody, Natural Killer Cell and Immune Mediator Profiles in Autoimmune Thyroid Diseases.

Tiphaine C Martin, Kristina M Ilieva, Alessia Visconti, Michelle Beaumont, Steven J Kiddle, Richard J B Dobson, Massimo Mangino, Ee Mun Lim, Marija Pezer, Claire J Steves and 7 more

Open access · goldAbstract read
In one paragraph

Article in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 2 pooled it
2.1field-weighted citation impact, top 10% 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

20 citing papers in PubMed, 2 syntheses or guidelines pooled it, 28 citations in OpenAlex.

  1. Pooled it
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  13. Generation and Characterization of Native and Sialic Acid-Deficient IgE.International journal of molecular sciences · 2022
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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

17 authors at 5 institutions in 4 countries.

Tiphaine C MartinDepartment of Twin Research and Genetic Epidemiology, King's College, London SE1 7EH, UK.ORCID 0000-0001-9990-1455
Kristina M IlievaSt John's Institute of Dermatology, School of Basic & Medical Biosciences, King's College London, Guy's Hospital, London SE1 9RT, UK.
Alessia ViscontiDepartment of Twin Research and Genetic Epidemiology, King's College, London SE1 7EH, UK.ORCID 0000-0003-4144-2019
Michelle BeaumontDepartment of Twin Research and Genetic Epidemiology, King's College, London SE1 7EH, UK.
Steven J KiddleDepartment of Biostatistics and Health Informatics, Institute of Psychiatry, Psychology and Neuroscience, King's College, London SE5 8AF, UK.
Richard J B DobsonDepartment of Biostatistics and Health Informatics, Institute of Psychiatry, Psychology and Neuroscience, King's College, London SE5 8AF, UK.ORCID 0000-0003-4224-9245
Massimo ManginoDepartment of Twin Research and Genetic Epidemiology, King's College, London SE1 7EH, UK.
Ee Mun LimDepartment of Endocrinology and Diabetes, Sir Charles Gairdner Hospital, Nedlands, WA 6009, Australia.
Marija PezerGenos, Glycoscience Research Laboratory, 10000 Zagreb, Croatia.
Claire J StevesDepartment of Twin Research and Genetic Epidemiology, King's College, London SE1 7EH, UK.ORCID 0000-0002-4910-0489
Jordana T BellDepartment of Twin Research and Genetic Epidemiology, King's College, London SE1 7EH, UK.ORCID 0000-0002-3858-5986
Scott G WilsonDepartment of Twin Research and Genetic Epidemiology, King's College, London SE1 7EH, UK.ORCID 0000-0002-0357-1373
Gordan LaucGenos, Glycoscience Research Laboratory, 10000 Zagreb, Croatia.
Mario RoedererImmunoTechnology Section, Vaccine Research Center, NIAID, NIH, Bethesda, MD 20892, USA.
John P WalshDepartment of Endocrinology and Diabetes, Sir Charles Gairdner Hospital, Nedlands, WA 6009, Australia.ORCID 0000-0002-1766-2612
Tim D SpectorDepartment of Twin Research and Genetic Epidemiology, King's College, London SE1 7EH, UK.
Sophia N KaragiannisSt John's Institute of Dermatology, School of Basic & Medical Biosciences, King's College London, Guy's Hospital, London SE1 9RT, UK.ORCID 0000-0002-4100-7810
King's College London · GBThe University of Western Australia · AUGuy's Hospital · GBGenos (Croatia) · HRUniversity of Zagreb · HR

Funding

Arthritis Research UKBritish Heart FoundationCancer Research UKChief Scientist OfficeDepartment of Health 05/40/04Department of Health RP-PG-0407-10314Medical Research Council MC_PC_13041Medical Research Council MC_PC_17214Medical Research Council MR/K006584/1Medical Research Council MR/L011859/1Medical Research Council MR/L023091/1Medical Research Council MR/P021573/1Medical Research Council PG 1087407Wellcome Trust
6 · The paper itself

Abstract

The pathogenesis of autoimmune thyroid diseases (AITD) is poorly understood and the association between different immune features and the germline variants involved in AITD are yet unclear. We previously observed systemic depletion of IgG core fucosylation and antennary α1,2 fucosylation in peripheral blood mononuclear cells in AITD, correlated with anti-thyroid peroxidase antibody (TPOAb) levels. Fucose depletion is known to potentiate strong antibody-mediated NK cell activation and enhanced target antigen-expressing cell killing. In autoimmunity, this may translate to autoantibody-mediated immune cell recruitment and attack of self-antigen expressing normal tissues. Hence, we investigated the crosstalk between immune cell traits, secreted proteins, genetic variants and the glycosylation patterns of serum IgG, in a multi-omic and cross-sectional study of 622 individuals from the TwinsUK cohort, 172 of whom were diagnosed with AITD. We observed associations between two genetic variants (rs505922 and rs687621), AITD status, the secretion of Desmoglein-2 protein, and the profile of two IgG N-glycan traits in AITD, but further studies need to be performed to better understand their crosstalk in AITD. On the other side, enhanced afucosylated IgG was positively associated with activatory CD335

Indexed as

AutoantibodiesCross-Sectional StudiesFucoseHumansIodide PeroxidaseKiller Cells, NaturalLeukocytes, MononuclearThyroid DiseasesAutoantibodiesFucoseIodide Peroxidasethyroid microsomal antibodiesantibody-dependent cell-mediated cytotoxicity (ADCC)anti-thyroid peroxidase antibody (TPOAb)apoptosisautoimmune thyroid diseases (AITD)genetic variantsmulti-omic

Identifiers

PMID32182948
PMCPMC7140647
OpenAlexW3009531907

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.