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Start Over Author "Blüml Stephan" Journal nature immunology
4 results on '"Blüml Stephan"'

2. Chronic signaling via the metabolic checkpoint kinase mTORC1 induces macrophage granuloma formation and marks sarcoidosis progression

Author

Linke, Monika, primary, Pham, Ha Thi Thanh, additional, Katholnig, Karl, additional, Schnöller, Thomas, additional, Miller, Anne, additional, Demel, Florian, additional, Schütz, Birgit, additional, Rosner, Margit, additional, Kovacic, Boris, additional, Sukhbaatar, Nyamdelger, additional, Niederreiter, Birgit, additional, Blüml, Stephan, additional, Kuess, Peter, additional, Sexl, Veronika, additional, Müller, Mathias, additional, Mikula, Mario, additional, Weckwerth, Wolfram, additional, Haschemi, Arvand, additional, Susani, Martin, additional, Hengstschläger, Markus, additional, Gambello, Michael J, additional, and Weichhart, Thomas, additional

Published
2017
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3. Regulation of autoantibody activity by the IL-23–TH17 axis determines the onset of autoimmune disease

Author

Pfeifle, René, primary, Rothe, Tobias, additional, Ipseiz, Natacha, additional, Scherer, Hans U, additional, Culemann, Stephan, additional, Harre, Ulrike, additional, Ackermann, Jochen A, additional, Seefried, Martina, additional, Kleyer, Arnd, additional, Uderhardt, Stefan, additional, Haugg, Benjamin, additional, Hueber, Axel J, additional, Daum, Patrick, additional, Heidkamp, Gordon F, additional, Ge, Changrong, additional, Böhm, Sybille, additional, Lux, Anja, additional, Schuh, Wolfgang, additional, Magorivska, Iryna, additional, Nandakumar, Kutty S, additional, Lönnblom, Erik, additional, Becker, Christoph, additional, Dudziak, Diana, additional, Wuhrer, Manfred, additional, Rombouts, Yoann, additional, Koeleman, Carolien A, additional, Toes, René, additional, Winkler, Thomas H, additional, Holmdahl, Rikard, additional, Herrmann, Martin, additional, Blüml, Stephan, additional, Nimmerjahn, Falk, additional, Schett, Georg, additional, and Krönke, Gerhard, additional

Published
2016
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4. Regulation of autoantibody activity by the IL-23-T H 17 axis determines the onset of autoimmune disease.

Author

Pfeifle R, Rothe T, Ipseiz N, Scherer HU, Culemann S, Harre U, Ackermann JA, Seefried M, Kleyer A, Uderhardt S, Haugg B, Hueber AJ, Daum P, Heidkamp GF, Ge C, Böhm S, Lux A, Schuh W, Magorivska I, Nandakumar KS, Lönnblom E, Becker C, Dudziak D, Wuhrer M, Rombouts Y, Koeleman CA, Toes R, Winkler TH, Holmdahl R, Herrmann M, Blüml S, Nimmerjahn F, Schett G, and Krönke G

Subjects
Animals, Cell Differentiation, Cells, Cultured, Disease Models, Animal, Glycosylation, Humans, Interleukins metabolism, Lymphocyte Activation, Mice, Mice, Inbred C57BL, Sialyltransferases genetics, Sialyltransferases metabolism, Signal Transduction, beta-D-Galactoside alpha 2-6-Sialyltransferase, Interleukin-22, Interleukin-21, Arthritis, Rheumatoid immunology, Autoantibodies metabolism, B-Lymphocytes immunology, Immune Tolerance, Immunoglobulin G metabolism, Interleukin-23 metabolism, Th17 Cells immunology
Abstract

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 H 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 H 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 H 17 cell-dependent pathway that controls autoantibody activity and unmasks a preexisting breach in immunotolerance., Competing Interests: The authors declare no competing financial interests.

Published
2017
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