Barone F Nayar S Campos J Cloake T Withers DR Toellner KM Zhang Y Fouser L Fisher B Bowman S Rangel-Moreno J Garcia-Hernandez Mde L Randall TD Lucchesi D Bombardieri M Pitzalis C Luther SA Buckley CD 2015 The series of events leading to tertiary lymphoid organ (TLO) formation in mucosal organs following tissue damage remain unclear. Using a virus-induced model of autoantibody formation in the salivary glands of adult mice, we demonstrate that IL-22 provides a mechanistic link between mucosal infection, B-cell recruitment, and humoral autoimmunity. IL-22 receptor engagement is necessary and sufficient to promote differential expression of chemokine (C-X-C motif) ligand 12 and chemokine (C-X-C motif) ligand 13 in epithelial and fibroblastic stromal cells that, in turn, is pivotal for B-cell recruitment and organization of the TLOs. Accordingly, genetic and therapeutic blockade of IL-22 impairs and reverses TLO formation and autoantibody production. Our work highlights a critical role for IL-22 in TLO-induced pathology and provides a rationale for the use of IL-22-blocking agents in B-cell-mediated autoimmune conditions. application/pdf https://sonar.ch/global/documents/238958 eng info:eu-repo/semantics/altIdentifier/doi/10.1073/pnas.1503315112 info:eu-repo/semantics/altIdentifier/pmid/26286991 info:eu-repo/semantics/openAccess Proceedings of the National Academy of Sciences of the United States of America. - 2015 IL-22 Sjogren's syndrome autoimmunity chemokines tertiary lymphoid organs Animals Autoantibodies B-Lymphocytes Chemokines, CXC Interleukins Lymphoid Tissue Mice Mice, Knockout IL-22 regulates lymphoid chemokine production and assembly of tertiary lymphoid organs. http://purl.org/coar/resource_type/c_6501