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However, whether they initiate autoimmune disease or perpetuate disease progression in terms of epiphenomena remains undefined.<\/jats:p>\n               <jats:p>Here, we show that depletion of MCPIP1 in macrophages and granulocytes (Mcpip1fl\/fl-LysMcre+ C57BL\/6 mice) is sufficient to trigger severe autoimmune disease. This was evidenced by the expansion of B cells and plasma cells and spontaneous production of autoantibodies, including anti-dsDNA, anti-Smith and anti-histone antibodies. Consequently, we document evidence of severe skin inflammation, pneumonitis and histopathologic evidence of glomerular IgG deposits alongside mesangioproliferative nephritis in 6-month-old mice. These phenomena are related to systemic autoinflammation, which secondarily induces a set of cytokines such as Baff, Il5, Il9 and Cd40L, affecting adaptive immune responses. Therefore, abnormal macrophage activation is a key factor involved in the loss of immune tolerance.<\/jats:p>\n               <jats:p>Overall, we demonstrate that deficiency of MCPIP1 solely in myeloid cells triggers systemic lupus-like autoimmunity and that the control of myeloid cell activation is a crucial checkpoint in the development of systemic autoimmunity.<\/jats:p>","DOI":"10.1242\/dmm.047589","type":"journal-article","created":{"date-parts":[[2021,3,18]],"date-time":"2021-03-18T12:25:14Z","timestamp":1616070314000},"source":"Crossref","is-referenced-by-count":21,"title":["Murine myeloid cell MCPIP1 suppresses autoimmunity by regulating B-cell expansion and differentiation"],"prefix":"10.1242","volume":"14","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-0151-9723","authenticated-orcid":false,"given":"Ewelina","family":"Dobosz","sequence":"first","affiliation":[{"name":"Department of Microbiology, Faculty of Biochemistry Biophysics and Biotechnology, Jagiellonian 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