According to a recent model, glycosylation of IgG is immunologically regulated, and the lower sialylation of IgG in RA is a result of the enhanced number/function of follicular T (Tfh) cells, and, in particular, Tfh17 cells downregulating sialyltransferase β-galactoside α-2,6-sialyltransferase 1 (ST6Gal I) in autoantibody-producing B cells. Here, ST6GAL1 is linked to rheumatoid arthritis.