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Ro52\/SSA, also denoted tripartite motif (TRIM)21, is a major autoantigen in Sj\u00f6gren's syndrome and systemic lupus erythematosus. Interestingly, TRIM21-deficient mice develop systemic autoimmunity with B cell-driven manifestations such as autoantibodies, hypergammaglobulinaemia and glomerulonephritis following tissue injury. The mechanisms by which TRIM21-deficiency leads to enhanced B cell activation and antibody production are, however, not well understood, and to further elucidate the role of TRIM21 in systemic autoimmunity, we investigated the B cell phenotype and antibody responses of Trim21\u2212\/\u2212 mice following immunization with thymus-dependent (TD) and thymus-independent (TI) antigens. We found that TRIM21-deficient mice developed significantly higher specific antibody titres than their wild-type counterparts upon B cell receptor (BCR) engagement by TD and TI type II antigens, and this was accompanied by an altered B cell phenotype. Furthermore, BCR cross-linking, but not anti-CD40 stimulation, in vitro resulted in a significantly higher proliferation of Trim21\u2212\/\u2212 cells. We also observed that splenic follicular B cells were expanded not only in immunized mice but also already in young, unmanipulated Trim21\u2212\/\u2212 mice, and transcriptomic analysis of these cells revealed an up-regulation of genes associated with B cell differentiation, indicating a role for TRIM21 in their regulation. In conclusion, in this study we describe a link between the rheumatic autoantigen Ro52\/TRIM21 and increased antibody production associated with follicular B cell expansion, implicating a potential role for Ro52\/TRIM21 in the pathogenesis of systemic autoimmune diseases.<\/jats:p>","DOI":"10.1111\/cei.13211","type":"journal-article","created":{"date-parts":[[2018,9,4]],"date-time":"2018-09-04T05:53:21Z","timestamp":1536040401000},"page":"315-326","source":"Crossref","is-referenced-by-count":28,"title":["The Sj\u00f6gren's syndrome-associated autoantigen Ro52\/TRIM21 modulates follicular B cell homeostasis and immunoglobulin production"],"prefix":"10.1093","volume":"194","author":[{"given":"S","family":"Brauner","sequence":"first","affiliation":[{"name":"Division of Rheumatology, Department of Medicine, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden"},{"name":"Neuroimmunology Unit, Department of Clinical Neurosciences, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M","family":"Ivanchenko","sequence":"additional","affiliation":[{"name":"Division of Rheumatology, Department of Medicine, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"G E","family":"Thorlacius","sequence":"additional","affiliation":[{"name":"Division of Rheumatology, Department of Medicine, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A","family":"Ambrosi","sequence":"additional","affiliation":[{"name":"Division of Rheumatology, Department of Medicine, Karolinska University Hospital, Karolinska Institutet, Stockholm, 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