The role of the IL-23/Th17 axis as modulator of B cell-mediated (auto)immune responses

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Our previously published data point towards a key role of the IL-23/Th17 axis as modulator of B cell-mediated Immunoglobulin G (IgG) glycosylation, IgG activity and plasmablast expansion. Additional preliminary data show a differential expression and regulation of the IL-17 Receptor (R), IL-22R and GMCSFR on B cells during B cell activation and during autoimmune disease. Together these data suggest that Th17-derived signals directly or indirectly affect key steps of the B cell and plasma cell response, although underlying mechanisms and consequences remain elusive. In the proposed project we therefore plan to expand our analyses and to address the global impact of the IL-23/Th17 axis on B cell biology and B cell-mediated autoimmune diseases. In particular, we aim to further identify involved cytokines and delineate underlying molecular mechanisms that mediate Th17 cell/B cell crosstalk in order to determine novel targets for the therapy of autoimmune and chronic inflammatory diseases.