Celiac.com 03/05/2010 - A team of researchers recently studied therelationship between increased levels of antigliadin antibodies andintestinal barrier gene variants.
The research team included V.M. Wolters, B. Z. Alizadeh, M. E. Weijerman, A. Zhernakova, I. M. vanHoogstraten, M. L. Mearin, M. C. Wapenaar, C.Wijmenga, M. W. Schreurs.They are affiliated with the Department of Pediatric Gastroenterology,UMC Utrecht, Utrecht, The Netherlands.
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Numerous genes may affectintestinal barrier function, including MAGI2, MYO9B, and PARD3, whichhave a close association with celiac disease. Gauging intestinalpermeability is tough to do, so researchers can test indirectly byusing antibodies against gliadin and Baker's yeast (anti-Saccharomycescerevisiae antibodies).
The goal of the study was to determinewhether intestinal permeability, represented by antibodies againstgliadin, was connected to MAGI2, MYO9B, and PARD3.
The teamanalyzed patients with Down syndrome, a population with suspectedincreased intestinal permeability. The team examined connectionsbetween AGA and ASCA.
The team genotyped 126 Down syndromepatients for six single-nucleotide polymorphisms in MAGI2 (rs1496770,rs6962966, rs9640699), MYO9B (rs1457092, rs2305764), and PARD3(rs10763976).
They then performed an allele dosage associationof these risk genes and AGA levels. They also found a strongcorrelation between AGA and ASCA (p < 0.01).
Subjects withone or more risk genotypes showed lower average AGA levels (trend testp = 0.007) and made up a larger number of patients with normal AGAlevels (p = 9.3 x 10(-5)).
Celiac-associated risk genotypesare associated with lower AGA values rather than higher AGA values.This all means that, regarding the increased prevalence of elevated AGAin patients with Down syndrome, there are other immunologic factors atplay. These may involve altered induction and/or maintenance oftolerance.
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