Evidence map›Paper›PMID 20737202›Full record

ArticleJournal of clinical immunology2010

Profile of autoantibodies against phosphorylcholine and cross-reactivity to oxidation-specific neoantigens in selective IgA deficiency with or without autoimmune diseases.

Ana Elisa Fusaro, Kristine Fahl, Elaine Cristina Cardoso, Cyro Alves de Brito, Cristina M A Jacob, Magda Carneiro-Sampaio, Alberto J S Duarte, Maria Notomi Sato

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Article in Journal of clinical immunology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

4 citing papers in PubMed, 10 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

8 authors at 2 institutions in 2 countries.

Ana Elisa FusaroLaboratório de Investigação em Dermatologia e Imunodeficiências, LIM 56, Faculdade de Medicina da USP, Instituto de Medicina Tropical de São Paulo, São Paulo, Brazil.
Kristine Fahl
Elaine Cristina Cardoso
Cyro Alves de Brito
Cristina M A Jacob
Magda Carneiro-Sampaio
Alberto J S Duarte
Maria Notomi Sato
Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo · BRInstituto de Medicina Tropical · PY

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immunoglobulin A deficiency (IgAD) is considered the most common form of primary immunodeficiency. The majority of IgA-deficient individuals are considered asymptomatic, even though IgAD has been associated with an increased frequency of recurrent infections, allergy, and autoimmune diseases. In this study we evaluate the Natural autoantibodies (NatAbs) reactivity to phosphorylcholine (PC) and to some pro-inflammatory molecules in IgAD with or without autoimmune disorders. We observed that in the absence of IgA there is an enhancement of IgG subclasses functioning as NatAbs against PC. Immunoglobulin G (IgG) against lipopolysaccharide, C-reactive protein, and IgA was found in IgAD, regardless of the autoimmune manifestations. Nonetheless, IgAD patients with autoimmune disease showed significantly higher IgG reactivity against pro-inflammatory molecules, such as cardiolipin, oxidized low-density lipoproteins, and phosphatidylserine, with positive correlation between them. In conclusion, the IgG NatAbs against PC may represent a compensatory defense mechanism against infections and control excess of inflammation, explaining the asymptomatic status in the IgA deficiency.

Indexed as

Cross ReactionsAdolescentAdultAutoantibodiesAutoantigensAutoimmune DiseasesChildFemaleHumansIgA DeficiencyImmunoglobulin GMaleMiddle AgedOxidation-ReductionPhosphorylcholineAutoantibodiesAutoantigensImmunoglobulin GPhosphorylcholine

Identifiers

PMID20737202
OpenAlexW1982282116

What OpenQuestion holds

Textmetadata
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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.