Author:
Martin Tiphaine C.,Šimurina Mirna,Ząbczyńska Marta,Kavur Marina Martinić,Rydlewska Magdalena,Pezer Marija,Kozłowska Kamila,Burri Andrea,Vilaj Marija,Turek-Jabrocka Renata,Krnjajić-Tadijanović Milena,Trofimiuk-Müldner Małgorzata,Lityńska Anna,Hubalewska-Dydejczyk Alicja,Trbojević-Akmačić Irena,Lim Ee Mun,Walsh John P.,Pochec Ewa,Spector Tim D.,Wilson Scott G.,Lauc Gordan
Abstract
AbstractAutoimmune thyroid diseases (AITD) are the most common group of autoimmune diseases, associated with lymphocyte infiltration and the production of thyroid autoantibodies, like thyroid peroxidase antibodies (TPOAb), in the thyroid gland. Immunoglobulins (Igs) and cell-surface receptors are glycoproteins with distinctive glycosylation patterns that play a structural role in maintaining and modulating their functions. We investigated associations of total circulating IgG and peripheral blood mononuclear cells (PBMCs) glycosylation with AITD and the influence of genetic background. The study revealed an inverse association of IgG core fucosylation with TPOAb and PBMCs antennary α1,2 fucosylation with AITD, but no shared genetic variance between AITD and glycosylation. These data suggest that the decreased level of IgG core fucosylation is a risk factor for AITD that promotes antibody-dependent cell-mediated cytotoxicity (ADCC) associated with TPOAb levels.
Publisher
Cold Spring Harbor Laboratory
Cited by
5 articles.
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