Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 23, Issue 5, Pages -Publisher
MDPI
DOI: 10.3390/ijms23052498
Keywords
celiac disease; deamidated gliadin peptides; transglutaminase antibody
Funding
- NKFI [120392, EFOP-3.6.1-16-2016-00022]
- European Union
- European Social Fund
- Interreg Danube CD SKILLS project [DTP3-571-1.2]
- Hungarian State
- Country of Lower Austria
- LMU Munich, Germany
- European Commission [FP6-2005-FOOD-4B-36383-PREVENTCD]
- Azrieli Foundation
- Deutsche Zoliakie Gesellschaft, Eurospital, Fondazione Celiachia, Fria Brod Sweden, Instituto de Salud Carlos III, Spanish Society for Pediatric Gastroenterology, Hepatology
- Nutrition, Komitet Badan Naukowych [1715/B/P01/2008/34]
- Fundacja Nutricia [1W44/FNUT3/2013]
- Stichting Coeliakie Onderzoek Nederland, Thermo Fisher Scientific
- European Society for Pediatric Gastroenterology, Hepatology
- Nutrition (ESPGHAN)
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Celiac disease is an autoimmune disorder characterized by immune response and antibody production to gluten. TG2 plays a role in the pathomechanism of celiac disease. This study investigates early antibody responses to reveal the development of celiac disease.
Celiac disease (CeD) is a conditional autoimmune disorder with T cell-mediated immune response to gluten coupled with antibody production to gliadin and the self-protein tissue transglutaminase (TG2). TG2 contributes to the CeD pathomechanism by deamidating gliadin, thereby generating more immunogenic peptides. Anti-gliadin antibodies may appear before the autoantibody production. The scope of this study was to dissect these early antibody responses by investigating serum samples collected during the PreventCD prospective double-blind study, where infants with high CeD risk were randomized to 200 mg daily gluten intake or placebo from 4 to 6 months of age, followed by frequent blood testing on regular gluten consumption in both groups. After primary gluten intake, children with or without later CeD produced IgA and IgG antibodies which preferentially recognized non-deamidated gliadin peptides. At CeD development with anti-TG2 seroconversion, there was a significant increase in the antibody reaction toward deamidated gliadin peptides (DGP), with maturation in the binding strength for the PEQPFP gamma-gliadin core peptide. The earliest produced autoantibodies targeted TG2's celiac epitope 2. Our results reveal a qualitative change in the gliadin-directed humoral immune response at the time when anti-TG2 antibodies appear, but anti-DGP antibodies in the absence of anti-TG2 antibodies are not disease-predictive.
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