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 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 glycosylation with AITD and the influence of genetic background in a case-control study with several independent cohorts and over 3,000 individuals in total. The study revealed an inverse association of IgG core fucosylation with TPOAb and AITD, as well as decreased peripheral blood mononuclear cells antennary α1,2 fucosylation in 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 previously associated with TPOAb levels.
Highlights
Autoimmune thyroid diseases (AITD) are a class of chronic, organ-specific autoimmune disorders that disturb the function of the thyroid gland
thyroid peroxidase antibodies (TPOAb) level and AITD are associated with a decreased level of Immunoglobulin G (IgG) core fucosylation The presence of autoimmune antibodies is not a definite sign of the AITD, so we wanted to test whether IgG glycosylation status can play a role in active AITD and correlated with the TPOAb level or AITD
We investigated the associations between total plasma IgG glycome composition and peripheral blood TPOAb level and AITD status in 2,297 (988 controls and 1309 TPOAb positive) and 1,191 individuals (988 controls and 203 AITD) respectively from the TwinsUK cohort (Discovery Cohort; Supplementary Table 1) using hydrophilic interaction chromatography ultraperformance liquid chromatography (HILIC UPLC)
Summary
Autoimmune thyroid diseases (AITD) are a class of chronic, organ-specific autoimmune disorders that disturb the function of the thyroid gland. They affect close to 5% of the European population (with a gender disparity) and so, represent the most common group of autoimmune diseases[1]. Except for antibodies against TSH receptors (TSAb), which are known to stimulate the production of thyroid hormones by binding TSH receptors in GD2, little is known about the role of two other thyroid autoantibodies, thyroid peroxidase antibodies (TPOAb) and thyroglobulin antibodies (TgAb). It is yet to be determined if anti-thyroid antibodies cause AITD, or whether additional control mechanisms, such as post-translational modifications, are required to trigger the disease onset
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