Evidence map›Paper›PMID 30177930›Full record

ArticleFrontiers in immunology2018

The Rare Anaphylaxis-Associated FcγRIIa3 Exhibits Distinct Characteristics From the Canonical FcγRIIa1.

Jessica C Anania, Halina M Trist, Catherine S Palmer, Peck Szee Tan, Betty P Kouskousis, Alicia M Chenoweth, Stephen J Kent, Graham A Mackay, Alberta Hoi, Rachel Koelmeyer and 7 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 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

6 citing papers in PubMed, 7 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

17 authors at 7 institutions in 1 country.

Jessica C AnaniaImmune Therapies Group, Burnet Institute, Melbourne, VIC, Australia.
Halina M TristImmune Therapies Group, Burnet Institute, Melbourne, VIC, Australia.
Catherine S PalmerImmune Therapies Group, Burnet Institute, Melbourne, VIC, Australia.
Peck Szee TanImmune Therapies Group, Burnet Institute, Melbourne, VIC, Australia.
Betty P KouskousisImmune Therapies Group, Burnet Institute, Melbourne, VIC, Australia.
Alicia M ChenowethImmune Therapies Group, Burnet Institute, Melbourne, VIC, Australia.
Stephen J KentDepartment of Microbiology and Immunology, University of Melbourne, Parkville, VIC, Australia.
Graham A MackayDepartment of Pharmacology & Therapeutics, The University of Melbourne, Parkville, VIC, Australia.
Alberta HoiDepartment of Medicine, Monash Medical Centre, Clayton, VIC, Australia.
Rachel KoelmeyerDepartment of Medicine, Monash Medical Centre, Clayton, VIC, Australia.
Charlotte SladeDepartment of Medical Biology, The University of Melbourne, Parkville, VIC, Australia.
Vanessa L BryantDepartment of Medical Biology, The University of Melbourne, Parkville, VIC, Australia.
Philip D HodgkinDepartment of Medical Biology, The University of Melbourne, Parkville, VIC, Australia.
Pei Mun AuiDepartment of Immunology and Pathology, Central Clinical School, Monash University, Melbourne, VIC, Australia.
Menno C van ZelmDepartment of Immunology and Pathology, Central Clinical School, Monash University, Melbourne, VIC, Australia.
Bruce D WinesImmune Therapies Group, Burnet Institute, Melbourne, VIC, Australia.
P Mark HogarthImmune Therapies Group, Burnet Institute, Melbourne, VIC, Australia.
Burnet Institute · AUMonash University · AUJeffrey Modell Foundation · AUMonash Medical Centre · AUWalter and Eliza Hall Institute of Medical Research · AUMelbourne Sexual Health Centre · AUUniversity of Melbourne · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

FcγRIIa is an activating FcγR, unique to humans and non-human primates. It induces antibody-dependent proinflammatory responses and exists predominantly as FcγRIIa1. A unique splice variant, we designated FcγRIIa3, has been reported to be associated with anaphylactic reactions to intravenous immunoglobulins (IVIg) therapy. We aim to define the functional consequences of this FcγRIIa variant associated with adverse responses to IVIg therapy and evaluate the frequency of associated SNPs. FcγRIIa forms from macaque and human PBMCs were investigated for IgG-subclass specificity, biochemistry, membrane localization, and functional activity. Disease-associated SNPs were analyzed by sequencing genomic DNA from 224 individuals with immunodeficiency or autoimmune disease. FcγRIIa3 was identified in macaque and human PBMC. The FcγRIIa3 is distinguished from the canonical FcγRIIa1 by a unique 19-amino acid cytoplasmic insertion and these two FcγRIIa forms responded distinctly to antibody ligation. Whereas FcγRIIa1 was rapidly internalized, FcγRIIa3 was retained longer at the membrane, inducing greater calcium mobilization and cell degranulation. Four

Indexed as

AnaphylaxisAnimalsBiomarkersCell DegranulationDisease SusceptibilityFluorescent Antibody TechniqueGene ExpressionGenetic LociHumansImmunoglobulin GLeukocytes, MononuclearMacacaMast CellsPhenotypePolymorphism, Single NucleotideProtein BindingBiomarkersFCGR2A protein, humanImmunoglobulin GProtein IsoformsReceptors, IgGcommon variable immunodeficiencyFc receptorsimmune compleximmunodeficiencynon-human primatessystemic lupus erythematosus

Identifiers

PMID30177930
PMCPMC6109644
OpenAlexW2885548301

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.