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However, the mechanism involved in AQP4-Ab production remains unclear.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Methods<\/jats:title>\n                <jats:p>We analyzed the immunophenotypes of patients with NMOSD and other neuroinflammatory diseases as well as healthy controls (HC) using flow cytometry. Transcriptome analysis of B cell subsets obtained from NMOSD patients and HCs was performed. The differentiation capacity of B cell subsets into antibody-secreting cells was analyzed.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Results<\/jats:title>\n                <jats:p>The frequencies of switched memory B (SMB) cells and plasmablasts were increased and that of na\u00efve B cells was decreased in NMOSD patients compared with relapsing\u2013remitting multiple sclerosis patients and HC. SMB cells from NMOSD patients had an enhanced potential to differentiate into antibody-secreting cells when cocultured with T peripheral helper cells. Transcriptome analysis revealed that the profiles of B cell lineage transcription factors in NMOSD were skewed towards antibody-secreting cells and that IL-2 signaling was upregulated, particularly in na\u00efve B cells. Na\u00efve B cells expressing CD25, a receptor of IL-2, were increased in NMOSD patients and had a higher potential to differentiate into antibody-secreting cells, suggesting CD25<jats:sup>+<\/jats:sup> na\u00efve B cells are committed to differentiate into antibody-secreting cells.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Conclusions<\/jats:title>\n                <jats:p>To the best of our knowledge, this is the first study to demonstrate that B cells in NMOSD patients are abnormally skewed towards antibody-secreting cells at the transcriptome level during the early differentiation phase, and that IL-2 might participate in this pathogenic process. Our study indicates that CD25<jats:sup>+<\/jats:sup> na\u00efve B cells are a novel candidate precursor of antibody-secreting cells in autoimmune diseases.<\/jats:p>\n              <\/jats:sec>","DOI":"10.1186\/s12974-021-02375-w","type":"journal-article","created":{"date-parts":[[2022,1,6]],"date-time":"2022-01-06T16:02:38Z","timestamp":1641484958000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":33,"title":["Dysregulated B cell differentiation towards antibody-secreting cells in neuromyelitis optica spectrum disorder"],"prefix":"10.1186","volume":"19","author":[{"given":"Yasunobu","family":"Hoshino","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daisuke","family":"Noto","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shuhei","family":"Sano","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuji","family":"Tomizawa","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kazumasa","family":"Yokoyama","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nobutaka","family":"Hattori","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6349-2936","authenticated-orcid":false,"given":"Sachiko","family":"Miyake","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2022,1,6]]},"reference":[{"key":"2375_CR1","doi-asserted-by":"publisher","first-page":"805","DOI":"10.1016\/S1474-4422(07)70216-8","volume":"6","author":"DM Wingerchuk","year":"2007","unstructured":"Wingerchuk DM, Lennon VA, Lucchinetti CF, Pittock SJ, Weinshenker BG. 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