{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T10:18:41Z","timestamp":1790763521270,"version":"4.1.0"},"reference-count":35,"publisher":"SAGE Publications","issue":"8","license":[{"start":{"date-parts":[[2020,9,14]],"date-time":"2020-09-14T00:00:00Z","timestamp":1600041600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Mult Scler"],"published-print":{"date-parts":[[2021,7]]},"abstract":"<jats:sec>\n                    <jats:title>Background:<\/jats:title>\n                    <jats:p>\n                      Multiple sclerosis (MS) is characterized by central nervous system (CNS) infiltration of T and B cells, excess inflammatory cytokine and chemokine production and failure of immune regulation. CD19+CD24\n                      <jats:sup>hi<\/jats:sup>\n                      CD38\n                      <jats:sup>hi<\/jats:sup>\n                      transitional B cells producing interleukin (IL)-10 have been shown to suppress interferon-\u03b3 (IFN\u03b3) and tumour necrosis factor-\u03b1 (TNF\u03b1) production by CD4+ T cells and to be dysfunctional in autoimmune arthritis and systemic lupus erythematosus.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective:<\/jats:title>\n                    <jats:p>We hypothesized that transitional B-cell-dependent immune regulation could be defective in MS and examined their function in healthy subjects and patients with relapsing-remitting multiple sclerosis (RRMS).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods:<\/jats:title>\n                    <jats:p>A total of 62 healthy donors and 21 RRMS subjects donated peripheral blood for the study. IL-10-producing B cells, IFN\u03b3 and TNF\u03b1-producing T cells and proliferating T cells were quantified by flow cytometry.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results:<\/jats:title>\n                    <jats:p>\n                      In healthy individuals, CD19+CD24\n                      <jats:sup>hi<\/jats:sup>\n                      CD38\n                      <jats:sup>hi<\/jats:sup>\n                      transitional B cells produce more IL-10 than CD19+CD24+CD38+ naive and CD19+CD24\n                      <jats:sup>hi<\/jats:sup>\n                      CD38\u2212 memory B cells and are able to suppress CD4+ T-cell proliferation and IFN\u03b3 and TNF\u03b1-production. In subjects with RRMS, CD19+CD24\n                      <jats:sup>hi<\/jats:sup>\n                      CD38\n                      <jats:sup>hi<\/jats:sup>\n                      transitional B cells produce significantly less IL-10 and to fail to suppress effector T-cell function.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion:<\/jats:title>\n                    <jats:p>\n                      CD19+CD24\n                      <jats:sup>hi<\/jats:sup>\n                      CD38\n                      <jats:sup>hi<\/jats:sup>\n                      transitional B cells physiologically represent the most potent regulatory B-cell subset and are functionally defective in patients with RRMS, an abnormality that may contribute to the immune pathological process.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1177\/1352458520951536","type":"journal-article","created":{"date-parts":[[2020,9,14]],"date-time":"2020-09-14T07:00:00Z","timestamp":1600066800000},"page":"1187-1197","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":40,"title":["Defective CD19+CD24\n                    <sup>hi<\/sup>\n                    CD38\n                    <sup>hi<\/sup>\n                    transitional B-cell function in patients with relapsing-remitting MS"],"prefix":"10.1177","volume":"27","author":[{"given":"Maria T","family":"Cencioni","sequence":"first","affiliation":[{"name":"Department of Brain Sciences, Imperial College London, London, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rehiana","family":"Ali","sequence":"additional","affiliation":[{"name":"Department of Brain Sciences, Imperial College London, London, 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