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. Author manuscript; available in PMC: 2021 Apr 2.
Published in final edited form as: Clin Rev Allergy Immunol. 2020 Nov 13;60(1):31–45. doi: 10.1007/s12016-020-08823-4

Fig. 2.

Fig. 2

IL-23/IL-17 axis contributes to autoantibody-driven diseases. B cells migrate between the dark and light zones of the germinal centers (GCs), a process mediated by CXCL12/CXCR4 and CXCL13/CXCR5, to undergo somatic hypermutation, clonal expansion, and affinity-based selection. Exposure to IL-17 reduces their migration which results in more rounds of somatic hypermutation and the production of IgG with increased affinity. Plasma cells emigrating from GCs produce autoantibodies. IL-23-activated TH17 cells suppress St6gal1 expression in antibody-producing cells via IL-21 and IL-22, which results in changes in the glycosylation profile as well as increased inflammatory activity of IgG (cDC: classical dendritic cells; FDC: follicular dendritic cells)