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Regulatory B cells inhibit EAE initiation in mice while other B cells promote disease progression
http://hdl.handle.net/2297/45128
http://hdl.handle.net/2297/45128e192ddd5-7fc1-4f58-9059-c287ad5005f1
名前 / ファイル | ライセンス | アクション |
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ME-PR-MATSUSHITA-T-3420.pdf (719.4 kB)
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Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2017-10-05 | |||||
タイトル | ||||||
タイトル | Regulatory B cells inhibit EAE initiation in mice while other B cells promote disease progression | |||||
言語 | ||||||
言語 | eng | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
資源タイプ | journal article | |||||
著者 |
Matsushita, Takashi
× Matsushita, Takashi× Yanaba, Koichi× Bouaziz, Jean-David× Fujimoto, Manabu× Tedder, Thomas F. |
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書誌情報 |
Journal of Clinical Investigation 巻 118, 号 10, p. 3420-3430, 発行日 2008-10-01 |
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ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 0021-9738 | |||||
NCID | ||||||
収録物識別子タイプ | NCID | |||||
収録物識別子 | AA00695520 | |||||
DOI | ||||||
関連タイプ | isIdenticalTo | |||||
識別子タイプ | DOI | |||||
関連識別子 | 10.1172/JCI36030 | |||||
出版者 | ||||||
出版者 | American Society for Clinical Investigation | |||||
抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | EAE is a mouse T cell-mediated autoimmune disease of the CNS used to model the human condition MS. The contributions of B cells to EAE initiation and progression are unclear. In this study, we have shown that EAE disease initiation and progression are differentially influenced by the depletion of B cells from mice with otherwise intact immune systems. CD20 antibody-mediated B cell depletion before EAE induction substantially exacerbated disease symptoms and increased encephalitogenic T cell influx into the CNS. Increased symptom severity resulted from the depletion of a rare IL-10-producing CD1d hiCD5+ regulatory B cell subset (B10 cells), since the adoptive transfer of splenic B10 cells before EAE induction normalized EAE in B cell-depleted mice. While transfer of regulatory B10 cells was maximally effective during early EAE initiation, they had no obvious role during disease progression. Rather, B cell depletion during EAE disease progression dramatically suppressed symptoms. Specifically, B cells were required for the generation of CD4+ T cells specific for CNS autoantigen and the entry of encephalitogenic T cells into the CNS during disease progression. These results demonstrate reciprocal regulatory roles for B cells during EAE immunopathogenesis. The therapeutic effect of B cell depletion for the treatment of autoimmunity may therefore depend on the relative contributions and the timing of these opposing B cell activities during the course of disease initiation and pathogenesis. | |||||
著者版フラグ | ||||||
出版タイプ | VoR | |||||
出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 |