{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,6]],"date-time":"2026-11-06T01:40:54Z","timestamp":1793929254725,"version":"4.8.0"},"reference-count":25,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2015,5,13]],"date-time":"2015-05-13T00:00:00Z","timestamp":1431475200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100004572","name":"National Health and Family Planning Commission of the People's Republic of China","doi-asserted-by":"publisher","award":["201402012"],"award-info":[{"award-number":["201402012"]}],"id":[{"id":"10.13039\/501100004572","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Scand J Immunol"],"published-print":{"date-parts":[[2015,6]]},"abstract":"Abstract<\/jats:title>\n \n The\n W<\/jats:styled-content>\n iskott\u2013\n A<\/jats:styled-content>\n ldrich syndrome protein (\n WAS<\/jats:styled-content>\n p) is an important regulator of the actin cytoskeleton and is required for immune cell function.\n WAS<\/jats:styled-content>\n p deficiency causes a marked reduction in major mature peripheral\n B<\/jats:styled-content>\n cell subsets, particularly marginal zone (\n MZ<\/jats:styled-content>\n )\n B<\/jats:styled-content>\n cells. We hypothesized that\n WAS<\/jats:styled-content>\n p deficiency may also lead to a reduction of regulatory\n B<\/jats:styled-content>\n cells (known as\n B<\/jats:styled-content>\n 10 cells) belonging to a novel subset of\n B<\/jats:styled-content>\n cells. And in consideration of the key role of\n B<\/jats:styled-content>\n 10 cells play in maintaining peripheral tolerance, we conjectured that a deficit of these cells could contribute to the autoimmunity in patients with\n W<\/jats:styled-content>\n iskott\u2013\n A<\/jats:styled-content>\n ldrich syndrome (\n WAS<\/jats:styled-content>\n ). The effects of\n WAS<\/jats:styled-content>\n p deficiency on\n B<\/jats:styled-content>\n 10 cells have been reported by only one group, which used an antigen\u2010induced arthritis model. To add more information, we measured the percentage of\n B<\/jats:styled-content>\n 10 cells, regulatory\n T<\/jats:styled-content>\n cells (\n T<\/jats:styled-content>\n regs) and\n T<\/jats:styled-content>\n h1 cells in\n WAS<\/jats:styled-content>\n p knockout (\n WAS<\/jats:styled-content>\n p\n KO<\/jats:styled-content>\n ) mice. We also measured the percentage of\n B<\/jats:styled-content>\n 10 cells in patients with\n WAS<\/jats:styled-content>\n by flow cytometry. Importantly, we used the non\u2010induced autoimmune\n WAS<\/jats:styled-content>\n p\n KO<\/jats:styled-content>\n mouse model to investigate the association between\n B<\/jats:styled-content>\n 10 cell frequency and the\n T<\/jats:styled-content>\n reg\/\n T<\/jats:styled-content>\n h1 balance. We found that the percentage of\n B<\/jats:styled-content>\n 10 cells was reduced in both mice (steady state and inflammatory state) and in humans and that the lower\n B<\/jats:styled-content>\n 10 population correlated with an imbalance in the\n T<\/jats:styled-content>\n reg\/\n T<\/jats:styled-content>\n h1 ratio in old\n WAS<\/jats:styled-content>\n p\n KO<\/jats:styled-content>\n mice with autoimmune colitis. These findings suggest that\n WAS<\/jats:styled-content>\n p plays a crucial role in\n B<\/jats:styled-content>\n 10 cell development and that\n WAS<\/jats:styled-content>\n p\u2010deficient\n B<\/jats:styled-content>\n 10 cells may contribute to autoimmunity in\n WAS<\/jats:styled-content>\n .\n <\/jats:p>","DOI":"10.1111\/sji.12282","type":"journal-article","created":{"date-parts":[[2015,2,26]],"date-time":"2015-02-26T15:28:54Z","timestamp":1424964534000},"page":"483-493","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":17,"title":["Effects of\n W<\/scp>\n iskott\u2013\n A<\/scp>\n ldrich Syndrome Protein Deficiency on\n IL<\/scp>\n \u201010\u2010Producing Regulatory B Cells in Humans and Mice"],"prefix":"10.1111","volume":"81","author":[{"given":"H.\u2010Q.","family":"Du","sequence":"first","affiliation":[{"name":"Ministry of Education Key Laboratory of Child Development and Disorders Children's Hospital of Chongqing Medical 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Hospital of Chongqing Medical University Chongqing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"X.\u2010D.","family":"Zhao","sequence":"additional","affiliation":[{"name":"Ministry of Education Key Laboratory of Child Development and Disorders Children's Hospital of Chongqing Medical University Chongqing China"},{"name":"Division of Immunology Children's Hospital of Chongqing Medical University Chongqing 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