Evidence map›Paper›PMID 32007544›Full record

ArticleTransplant immunology2020

Pre-existing self-reactive IgA antibodies associated with primary graft dysfunction after lung transplantation.

Vaidehi Kaza, Chengsong Zhu, Leying Feng, Fernando Torres, Srinivas Bollineni, Manish Mohanka, Amit Banga, John Joerns, T Mohanakumar, Lance S Terada and 1 more

Open access · greenAbstract read
In one paragraph

Article in Transplant immunology, 2020. 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
1.2field-weighted citation impact, top 22% 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, 9 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

11 authors at 2 institutions in 1 country.

Vaidehi KazaDivision of Pulmonary Critical Care, University of Texas Southwestern Medical Center, Dallas, TX 75390-8814, United States of America. Electronic address: Vaidehi.kaza@utsouthwestern.edu.
Chengsong ZhuDepartment of Immunology, Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, United States of America.
Leying FengDepartment of Immunology, Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, United States of America.
Fernando TorresDivision of Pulmonary Critical Care, University of Texas Southwestern Medical Center, Dallas, TX 75390-8814, United States of America.
Srinivas BollineniDivision of Pulmonary Critical Care, University of Texas Southwestern Medical Center, Dallas, TX 75390-8814, United States of America.
Manish MohankaDivision of Pulmonary Critical Care, University of Texas Southwestern Medical Center, Dallas, TX 75390-8814, United States of America.
Amit BangaDivision of Pulmonary Critical Care, University of Texas Southwestern Medical Center, Dallas, TX 75390-8814, United States of America.
John JoernsDivision of Pulmonary Critical Care, University of Texas Southwestern Medical Center, Dallas, TX 75390-8814, United States of America.
T MohanakumarNorton Thoracic Institute, St. Joseph's Hospital and Medical Center, Phoenix, AZ, United States of America.
Lance S TeradaDivision of Pulmonary Critical Care, University of Texas Southwestern Medical Center, Dallas, TX 75390-8814, United States of America.
Quan-Zhen LiDepartment of Immunology, Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, United States of America. Electronic address: quan.li@utsouthwestern.edu.
The University of Texas Southwestern Medical Center · USSt. Joseph's Hospital and Medical Center · US

Funding

(PQ1) Epigenetic effects of the premalignant fieldR01CA208620 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI TERADA, LANCE S · 2016 to 2020
$1.9M
NCI NIH HHS R01 CA208620
6 · The paper itself

Abstract

backgroundPrimary graft Dysfunction (PGD) results in significant mortality and morbidity after lung transplantation (LT). The objective of this study was to evaluate if pre-existing antibodies to self-antigens in sera of LT recipients are associated with PGD.

methodsThe serum profiles of IgG and IgA autoantibodies were analyzed using a customized proteomic microarray bearing 124 autoantigens. Autoantibodies were analyzed using Mann-Whitney U test or Fisher exact test. The association of the autoantibodies with clinical phenotypes and survival was analyzed by Kaplan-Meier Survival Analysis. Receiver operating curve characteristics (ROC) were calculated to evaluate the predictive value of the autoantibodies for PGD.

results51 patients were included in this study. Autoantigen microarray analysis on the pre-transplantation samples identified 17 IgA and 3 IgG autoantibodies which were significantly higher in recipients who developed PGD compared to those who did not (adjusted p < .05 and fold change>1.5). 6 IgA Abs were significantly associated with survival. Taken as a panel, an elevation of 6 IgA Abs had significant predictive value for PGD. Area under the curve value for the panel was 0.9413 for PGD with ROC analysis. Notably, 6 of the 17 IgA autoantigen targets are belong to proteoglycan family of extracellular matrix proteins.

conclusionPre-existing IgG and IgA autoantibodies in LT patients correlate with PGD and with survival in a single center, small cohort of lung transplant recipients. Further validation is needed to confirm the findings in the study.

Indexed as

Lung TransplantationAdultAgedAutoantibodiesAutoantigensFemaleHumansImmunoglobulin AMaleMiddle AgedPredictive Value of TestsPrimary Graft DysfunctionPrognosisRetrospective StudiesSurvival AnalysisAutoantibodiesAutoantigensImmunoglobulin AAutoantibodiesLung transplantationPrimary graft dysfunction

Identifiers

PMID32007544
PMCPMC7645846
OpenAlexW3003157710

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.