{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T23:35:46Z","timestamp":1791329746980,"version":"4.3.1"},"reference-count":41,"publisher":"SAGE Publications","issue":"2","license":[{"start":{"date-parts":[[2017,2,1]],"date-time":"2017-02-01T00:00:00Z","timestamp":1485907200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"funder":[{"DOI":"10.13039\/501100004008","name":"Istituto Superiore di Sanit\u00e0","doi-asserted-by":"publisher","award":["(to Eliana Marina Coccia)"],"award-info":[{"award-number":["(to Eliana Marina Coccia)"]}],"id":[{"id":"10.13039\/501100004008","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100007366","name":"Fondazione Italiana Sclerosi Multipla","doi-asserted-by":"publisher","award":["#2013\/R\/9 (to Eliana Marina Coccia)"],"award-info":[{"award-number":["#2013\/R\/9 (to Eliana Marina Coccia)"]}],"id":[{"id":"10.13039\/100007366","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100007366","name":"Fondazione Italiana Sclerosi Multipla","doi-asserted-by":"publisher","award":["#2014\/R\/19 (to Martina Severa)"],"award-info":[{"award-number":["#2014\/R\/19 (to Martina Severa)"]}],"id":[{"id":"10.13039\/100007366","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Mult Scler"],"published-print":{"date-parts":[[2018,2]]},"abstract":"<jats:sec>\n                    <jats:title>Background:<\/jats:title>\n                    <jats:p>B cells are key pathogenic effectors in multiple sclerosis (MS) and several therapies have been designed to restrain B cell abnormalities by directly targeting this lymphocyte population.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objectives:<\/jats:title>\n                    <jats:p>Moving from our data showing a Toll-like receptor (TLR)7-driven dysregulation of B cell response in relapsing\u2013remitting multiple sclerosis (RRMS) and having found a low serum level of Thymosin-\u03b11 (T\u03b11) in patients, we investigated whether the addition of this molecule to peripheral blood mononuclear cells (PBMCs) would influence the expansion of regulatory B cell subsets, known to dampen autoimmune inflammation.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods:<\/jats:title>\n                    <jats:p>Serum T\u03b11 level was measured by enzyme immunoassay. Cytokine expression was evaluated by Cytometric Bead Array (CBA), enzyme-linked immunosorbent assay (ELISA), and real-time reverse transcription polymerase chain reaction (RT-PCR). B cell subsets were analyzed by flow cytometry.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results:<\/jats:title>\n                    <jats:p>\n                      T\u03b11 pre-treatment induces an anti-inflammatory status in TLR7-stimulated RRMS PBMC cultures, reducing the secretion of pro-inflammatory interleukin (IL)-6, IL-8, and IL-1\u03b2 while significantly increasing the regulatory IL-10 and IL-35. Indeed, T\u03b11 treatment enhanced expansion of CD19\n                      <jats:sup>+<\/jats:sup>\n                      CD24\n                      <jats:sup>+<\/jats:sup>\n                      CD38\n                      <jats:sup>hi<\/jats:sup>\n                      transitional-immature and CD24\n                      <jats:sup>low\/neg<\/jats:sup>\n                      CD38\n                      <jats:sup>hi<\/jats:sup>\n                      plasmablast-like regulatory B cell subsets, which likely inhibit both interferon (IFN)-\u03b3 and IL-17 production.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion::<\/jats:title>\n                    <jats:p>Our study reveals a deficient ability of B cells from MS patients to differentiate into regulatory subsets and unveils a novel anti-inflammatory and repurposing potential for T\u03b11 in MS targeting B cell response.<\/jats:p>\n               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