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.
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.