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Pfeifle, René; Rothe, Tobias; Ipseiz, Natacha; Scherer, Hans U; Culemann, Stephan; Harre, Ulrike; Ackermann, Jochen A; Seefried, Martina; Kleyer, Arnd; Uderhardt, Stefan; Haugg, Benjamin; Hueber, Axel J; Daum, Patrick; Heidkamp, Gordon F; Ge, Changrong; Böhm, Sybille; Lux, Anja; Schuh, Wolfgang; Magorivska, Iryna; Nandakumar, Kutty S; Lönnblom, Erik; Becker, Christoph; Dudziak, Diana; Wuhrer, Manfred; Rombouts, Yoann; Koeleman, Carolien A; Toes, René; Winkler, Thomas H; Holmdahl, Rikard; Herrmann, Martin; Blüml, Stephan; Nimmerjahn, Falk; Schett, Georg; Krönke, Gerhard
Nature immunology, 01/2017, Letnik: 18, Številka: 1Journal Article
The checkpoints and mechanisms that contribute to autoantibody-driven disease are as yet incompletely understood. Here we identified the axis of interleukin 23 (IL-23) and the T 17 subset of helper T cells as a decisive factor that controlled the intrinsic inflammatory activity of autoantibodies and triggered the clinical onset of autoimmune arthritis. By instructing B cells in an IL-22- and IL-21-dependent manner, T 17 cells regulated the expression of β-galactoside α2,6-sialyltransferase 1 in newly differentiating antibody-producing cells and determined the glycosylation profile and activity of immunoglobulin G (IgG) produced by the plasma cells that subsequently emerged. Asymptomatic humans with rheumatoid arthritis (RA)-specific autoantibodies showed identical changes in the activity and glycosylation of autoreactive IgG antibodies before shifting to the inflammatory phase of RA; thus, our results identify an IL-23-T 17 cell-dependent pathway that controls autoantibody activity and unmasks a preexisting breach in immunotolerance.
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