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Increased Levels of Antigliadin Antibodies not Fully Explained by Intestinal Barrier Gene Variants

Celiac.com 03/05/2010 - A team of researchers recently studied the relationship between increased levels of antigliadin antibodies and intestinal barrier gene variants.

The research team included V. M. Wolters, B. Z. Alizadeh, M. E. Weijerman, A. Zhernakova, I. M. van Hoogstraten, 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.

Numerous genes may affect intestinal barrier function, including MAGI2, MYO9B, and PARD3, which have a close association with celiac disease. Gauging intestinal permeability is tough to do, so researchers can test indirectly by using antibodies against gliadin and Baker's yeast (anti-Saccharomyces cerevisiae antibodies).

The goal of the study was to determine whether intestinal permeability, represented by antibodies against gliadin, was connected to MAGI2, MYO9B, and PARD3.

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The team analyzed patients with Down syndrome, a population with suspected increased intestinal permeability. The team examined connections between AGA and ASCA.

The team genotyped 126 Down syndrome patients for six single-nucleotide polymorphisms in MAGI2 (rs1496770, rs6962966, rs9640699), MYO9B (rs1457092, rs2305764), and PARD3 (rs10763976).

They then performed an allele dosage association of these risk genes and AGA levels. They also found a strong correlation between AGA and ASCA (p < 0.01).

Subjects with one or more risk genotypes showed lower average AGA levels (trend test p = 0.007) and made up a larger number of patients with normal AGA levels (p = 9.3 x 10(-5)).

Celiac-associated risk genotypes are associated with lower AGA values rather than higher AGA values. This all means that, regarding the increased prevalence of elevated AGA in patients with Down syndrome, there are other immunologic factors at play. These may involve altered induction and/or maintenance of tolerance.

Source:
Hum Immunol. 2010 Feb 3.

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