Abstract :
Celiac disease (CD) is a chronic inflammatory
disease of the gut occurring in genetically
susceptible individuals after the ingestion of gluten. It
is characterized by a flattened mucosa, villous atrophy,
and crypt hyperplasia in the small intestine, by the
classic malabsorption syndrome (diarrhea, steatorrhea,
weight loss), or by seemingly less severe symptoms such
as iron deficiency anemia, osteopenic bone disease,
amenorrhea, and infertility (1). The elimination of
gluten from the diet generally leads to a return to
normality of the morphological changes (2). Intestinal
damage is caused by an interaction between the
deamidated glutamine residues of gliadin and HLADQ2
(DQA1*05/DQB1*2) or DQ8 (DQA1*03/
DQB1*0302) molecules (3), with consequent T-cell
response and production of autoantibodies against type
2 transglutaminase (anti-tTG2-Ab). HLA phenotype is
also considered the most important genetic marker of
nonresponders to the hepatitis B (HBV) vaccination.
In particular, the immune response to the HBV
vaccine is largely determined by the presence of the
immunogenetic peptides via the HLA-DR and DQ
molecules (4, 5), with the DR3-DQ2 and DR7-DQ2
haplotypes generally having a lower response rate (6-9).
