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Functional impairment of CD19 + CD24 hi CD38 hi B cells in neuromyelitis optica spectrum disorder is restored by B cell depletion therapy
DC Field | Value | Language |
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dc.contributor.author | 이은직 | - |
dc.date.accessioned | 2022-09-14T01:50:05Z | - |
dc.date.available | 2022-09-14T01:50:05Z | - |
dc.date.issued | 2021-12 | - |
dc.identifier.issn | 1946-6234 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/190638 | - |
dc.description.abstract | The role of B cells in immune response regulation is context dependent. In some cases, bystander B cell activation leads to interleukin-10 (IL-10) production, suppressing inappropriate immune responses. However, the role of B cells in regulation of autoimmune diseases, including neuromyelitis optica spectrum disorder (NMOSD), is incompletely understood. NMOSD is an autoimmune disease of the central nervous system with a relapsing-remitting course in which acute attacks lead to severe disability. B cell depletion therapy (BCDT) has shown clinical efficacy in NMOSD by eliminating pathogenic B cells; however, its effect on regulatory B (Breg) cells remains elusive. Here, we evaluated the B cell subsets, Breg cell function, and the effect of BCDT on these cells in patients with NMOSD. We showed that CD24hiCD38hi B cells from patients with NMOSD did not inhibit CD4+ T cell production of interferon-γ (IFN-γ), IL-17, or IL-21 and failed to inhibit follicular helper T cell expansion or induce regulatory T cells. This cellular impairment in patients with NMOSD can be explained by deficient Breg cell numbers and Breg cell–intrinsic deficits in IL-10 production specifically in response to B cell bystander activation. Using cross-sectional and 3-year longitudinal studies, we showed that BCDT treatment restored the numerical deficiency of Breg cells. Moreover, the post-BCDT repopulated CD24hiCD38hi B cells restored IL-10 production and suppressed IFN-γ and IL-17 production by CD4+ T cells. Our results suggest that both numerical deficiency of CD24hiCD38hi B cells and their impaired regulatory function contribute to NMOSD pathophysiology, and function is restored after BCDT. | - |
dc.description.statementOfResponsibility | restriction | - |
dc.language | English | - |
dc.publisher | American Association for the Advancement of Science | - |
dc.relation.isPartOf | SCIENCE TRANSLATIONAL MEDICINE | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.subject.MESH | Antigens, CD19 | - |
dc.subject.MESH | B-Lymphocytes, Regulatory* | - |
dc.subject.MESH | CD24 Antigen | - |
dc.subject.MESH | Cell Count | - |
dc.subject.MESH | Cross-Sectional Studies | - |
dc.subject.MESH | Humans | - |
dc.subject.MESH | Neuromyelitis Optica* / therapy | - |
dc.title | Functional impairment of CD19 + CD24 hi CD38 hi B cells in neuromyelitis optica spectrum disorder is restored by B cell depletion therapy | - |
dc.type | Article | - |
dc.contributor.college | College of Medicine (의과대학) | - |
dc.contributor.department | Dept. of Internal Medicine (내과학교실) | - |
dc.contributor.googleauthor | Yeseul Kim | - |
dc.contributor.googleauthor | So Yeon Kim | - |
dc.contributor.googleauthor | Sang-Min Han | - |
dc.contributor.googleauthor | Rosah May Payumo | - |
dc.contributor.googleauthor | Kevin Park | - |
dc.contributor.googleauthor | Ha Eun Kim | - |
dc.contributor.googleauthor | Su-Hyun Kim | - |
dc.contributor.googleauthor | Jae-Won Hyun | - |
dc.contributor.googleauthor | Eunjig Lee | - |
dc.contributor.googleauthor | Ho Jin Kim | - |
dc.identifier.doi | 10.1126/scitranslmed.abk2132 | - |
dc.contributor.localId | A03050 | - |
dc.relation.journalcode | J02645 | - |
dc.identifier.eissn | 1946-6242 | - |
dc.identifier.pmid | 34910550 | - |
dc.identifier.url | https://www.science.org/doi/10.1126/scitranslmed.abk2132 | - |
dc.contributor.alternativeName | Lee, Eun Jig | - |
dc.contributor.affiliatedAuthor | 이은직 | - |
dc.citation.volume | 13 | - |
dc.citation.number | 624 | - |
dc.citation.startPage | eabk2132 | - |
dc.identifier.bibliographicCitation | SCIENCE TRANSLATIONAL MEDICINE, Vol.13(624) : eabk2132, 2021-12 | - |
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