Typical features of
celiac disease are small-bowel villus
atrophy, crypt
hyperplasia, and
inflammation which develop gradually concomitant with ingestion of
gluten. In addition, patients have anti-
transglutaminase 2 (TG2)
autoantibodies in their serum and tissues. The aim of this study was to establish whether
celiac disease can be passively transferred to mice by serum or
immunoglobulins. Serum aliquots or purified
immunoglobulins (Ig) were intraperitoneally injected into Hsd:Athymic Nude-Foxn1nu mice for 8 or 27 days. As mice do not have proper
IgA transport from peritoneum to blood, sera with a high content of
IgG class anti-TG2
antibodies from untreated
IgA-deficient celiac patients were used. Mouse sera were tested for
celiac disease-specific
autoantibodies, and several tissues were analyzed for
autoantibody deposits targeted to TG2. Morphological assessment was made of the murine small intestinal mucosa. Injection of
celiac disease patient sera or total
IgG led to a significant delay in
weight gain and mild
diarrhea in a subset of mice. The mice injected with celiac patient sera or
IgG had significantly decreased villus height crypt depth (Vh/CrD) ratios and
celiac disease-specific
autoantibody deposits targeted to TG2 in several tissues, including the small intestine. None of these features were observed in control mice. We conclude that administration of
IgA-deficient
celiac disease patient serum or total
IgG induces both deterioration of the intestinal mucosa and clinical features of
celiac disease in mice. The experimentally induced condition in the mice injected with patient serum or
IgG resembles early developing
celiac disease in humans.
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