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Amelogenin specific IgA and IgG in children with untreated coeliac disease
Author(s) -
Petronijevic Sanja,
Stig Solveig,
Gao Jian,
Halstensen Trond S.
Publication year - 2016
Publication title -
european journal of oral sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.802
H-Index - 93
eISSN - 1600-0722
pISSN - 0909-8836
DOI - 10.1111/eos.12314
Subject(s) - amelogenin , gliadin , coeliac disease , immune system , saliva , immunoglobulin a , immunology , enamel paint , chemistry , immunoglobulin g , gluten , medicine , disease , dentistry , biochemistry
Children with untreated coeliac disease ( CD ) may develop enamel defects. Moreover, children with untreated CD have increased serum levels of gliadin reactive IgG, which may cross‐react to amelogenin. The aim of this study was to investigate reactivity of anti‐gliadin IgA and IgG to amelogenin in children with untreated CD . Blood samples from patients with CD ( n = 75) and from disease controls ( n = 24) were analysed for IgA and IgG reactivities to amelogenin (Emdogain) and to gliadin by ELISA . Whereas children with CD had statistically significantly higher serum levels of anti‐amelogenin IgA, only those with the most severe CD (Marsh 3c) had significantly higher anti‐amelogenin IgG immune reactivity than the disease controls. Western blotting confirmed that the IgA and IgG immune reactivity was to the amelogenin‐specific bands in Emdogain and to a 22‐ kD a human recombinant amelogenin. Cross‐inhibition studies revealed that the anti‐amelogenin immune reactivity was not only caused by anti‐gliadin cross‐reactivity but also included amelogenin selective immune reactivity. Some controls had high levels of anti‐amelogenin IgA and IgG, similar to children with CD . Thus, anti‐amelogenin IgA and IgG may not only be involved in the aetiology of CD ‐associated enamel defects but may also interfere with enamel maturation in non‐coeliac children.