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Although IL\u201022 is considered a pro\u2010inflammatory cytokine, its mechanism of action in RA remains incompletely understood. Here, we used the collagen\u2010induced arthritis model in IL\u201022 deficient (IL\u201022<jats:sup>\u2212\/\u2212<\/jats:sup>) mice to study the role of IL\u201022 in RA. In spite of normal disease incidence, disease severity is significantly diminished in IL\u201022<jats:sup>\u2212\/\u2212<\/jats:sup> mice. Moreover, pathogenicity of Th17 cells and development and function of B cells are unaffected. In contrast, splenic plasma cells, as well as serum autoantibody titers, are reduced in the absence of IL\u201022. At the peak of disease, germinal centers (GCs) are severely reduced in the spleens of IL\u201022<jats:sup>\u2212\/\u2212<\/jats:sup> mice, correlating with a decline in GC B\u2010cell numbers. Within the GC, we identified IL\u201022R1 expressing follicular dendritic cell\u2010like stromal cells. Human lymphoid stromal cells respond to IL\u201022 ex vivo by inducing transcription of CXCL12 and CXCL13. We therefore postulate IL\u201022 as an important enhancer of the GC reaction, maintaining chemokine levels for the persistence of GC reactions, essential for the production of autoantibody\u2010secreting plasma cells. Blocking IL\u201022 might therefore prevent immune\u2010complex deposition and destruction of joints in RA patients.<\/jats:p>","DOI":"10.1002\/eji.201546241","type":"journal-article","created":{"date-parts":[[2016,4,12]],"date-time":"2016-04-12T04:24:15Z","timestamp":1460435055000},"page":"1404-1414","source":"Crossref","is-referenced-by-count":29,"title":["Loss of IL\u201022 inhibits autoantibody formation in collagen\u2010induced arthritis in mice"],"prefix":"10.1002","volume":"46","author":[{"given":"Odilia B. 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