Decreased IgG core fucosylation, a player in antibody-dependent cell-mediated cytotoxicity, is associated with autoimmune thyroid diseases
T. C. Martin, M. Simurina, M. Zabczynska, M. Martinic Kavur, M. Rydlewska, M. Pezer, K. Kozlowska, A. Burri, M. Vilaj, R. Turek-Jabrocka, M. Krnjajic-Tadijanovic, M. Trofimiuk-Muldner, A. Litynska, A. Hubalewska-Dydejczyk, I. Trbojevic-Akmacic, E. Mun Lim, J. P. Walsh, E. Pochec, T. D. Spector, S. G. Willson, G. Lauc
Abstract
Autoimmune 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 1,2 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.
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