Evidence map›Paper›PMID 20007585›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2009

Dynamics of the interaction of human IgG subtype immune complexes with cells expressing R and H allelic forms of a low-affinity Fc gamma receptor CD32A.

Rangaiah Shashidharamurthy, Fang Zhang, Aaron Amano, Aparna Kamat, Ravichandran Panchanathan, Daniel Ezekwudo, Cheng Zhu, Periasamy Selvaraj

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.8field-weighted citation impact, top 7% 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

26 citing papers in PubMed, 50 citations in OpenAlex.

  1. Trial
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  10. The Neutrophil: The Underdog That Packs a Punch in the Fight against Cancer.International journal of molecular sciences · 2020
    Review
  11. Article
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  17. Monocyte recruitment by HLA IgG-activated endothelium: the relationship between IgG subclass and FcγRIIa polymorphisms.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2015
    Article
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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

8 authors at 2 institutions in 1 country.

Rangaiah ShashidharamurthyDepartment of Pathology and Laboratory Medicine, Emory University, Atlanta, GA 30322, USA.
Fang Zhang
Aaron Amano
Aparna Kamat
Ravichandran Panchanathan
Daniel Ezekwudo
Cheng Zhu
Periasamy Selvaraj
Emory University · USGeorgia Institute of Technology · US

Funding

Ligand Binding Kinetics and Cell Adhesion by Fc ReceptorR01AI038282 · NIAID · GEORGIA INSTITUTE OF TECHNOLOGY · PI ZHU, CHENG · 2001 to 2005
$1.9M
Regulation of CD32A in neutrophilsR01AI049400 · NIAID · EMORY UNIVERSITY · PI SELVARAJ, PERIASAMY · 2003 to 2007
$1.5M
Fc receptor targeted therapy for immune hemolytic anemiaR21HL091268 · NHLBI · EMORY UNIVERSITY · PI SELVARAJ, PERIASAMY · 2008 to 2009
$444k
NHLBI NIH HHS R21 HL091268NHLBI NIH HHS R21HL09126SNIAID NIH HHS R01 AI038282NIAID NIH HHS R01 AI049400NIAID NIH HHS R01 AI38282
6 · The paper itself

Abstract

CD32A, the major phagocytic FcgammaR in humans, exhibits a polymorphism in the ligand binding domain. Individuals homozygous for the R allelic form of CD32A (CD32A(R) allele) are more susceptible to bacterial infections and autoimmune diseases as compared with H allelic CD32A (CD32A(H)) homozygous and CD32A(R/H) heterozygous individuals. To understand the mechanisms behind this differential susceptibility, we have investigated the dynamics of the interaction of these allelic forms of CD32A when they are simultaneously exposed to immune complexes (IC). Binding studies using Ig fusion proteins of CD32A alleles showed that the R allele has significantly lower binding not only to human IgG2, but also to IgG1 and IgG3 subtypes. Competition assays using purified molecules demonstrated that CD32A(H)-Ig outcompetes CD32A(R)-Ig for IC binding when both alleles simultaneously compete for the same ligand. CD32A(H)-Ig blocked the IC binding mediated by both the allelic forms of cell surface CD32A, whereas CD32A(R)-Ig blocked only CD32A(R) and was unable to cross-block IC binding mediated by CD32A(H). Two-dimensional affinity measurements also demonstrated that CD32A(R) has significantly lower affinity toward all three subtypes as compared with CD32A(H). Our data suggest that the lower binding of CD32A(R) not only to IgG2 but also to IgG1 and IgG3 might be responsible for the lack of clearance of IC leading to increased susceptibility to bacterial infections and autoimmune diseases. Our data further suggests that in humans, inflammatory cells from CD32A(R/H) heterozygous individuals may predominantly use the H allele to mediate Ab-coated target cell binding during phagocytosis and Ab-dependent cellular cytotoxicity, resulting in a phenotype similar to CD32A(H) homozygous individuals.

Indexed as

AllelesAnimalsAntigen-Antibody ComplexArginineAutoimmune DiseasesBacterial InfectionsBinding, CompetitiveCell LineCell MembraneCHO CellsCricetinaeCricetulusDimerizationGenetic Predisposition to DiseaseHistidineHumansAntigen-Antibody ComplexArginineFc gamma receptor IIAHistidineImmunoglobulin GLigandsReceptors, IgGRecombinant Fusion Proteins

Identifiers

PMID20007585
PMCPMC2796592
OpenAlexW2123370587

What OpenQuestion holds

Textmetadata
LicenceTDM
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.