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. 2020 Feb 5;19(5):774–792. doi: 10.1074/mcp.RA119.001860

Fig. 5.

Fig. 5.

Hypothetic model of the possible role of the glycosylation of TPOAb driven by tissue-specific FUT8 and IKZF1 expression in AITD patients. Because of the lack of the significant deregulation of the expression of FUT8 and IKZF1 genes in whole blood of AITD patients, these genes could have an aberrant expression in a tissue-specific manner. It was previously suggested that TPOAb producing B-cells are generated in the germinal centers that are appearing in the thyroid gland of the AITD patients. Those cells could have aberrant expression of FUT8 and IKZF1 genes resulting in afucosylated (AF) TPOAb antibodies that are stimulating potentially harmful ADCC directed against the thyroid epithelial cells (thyrocytes), and therefore contributing to the AITD development.