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タイトル: | IRF-2 regulates B-cell proliferation and antibody production through distinct mechanisms. |
著者: | Minamino, Kento Takahara, Kazuhiko ![]() ![]() ![]() Adachi, Takumi Nagaoka, Koji Iyoda, Tomonori Taki, Shinsuke Inaba, Kayo ![]() |
著者名の別形: | 稲葉, カヨ |
キーワード: | activation antibody production B cells differentiation interferon regulatory factor-2 |
発行日: | 5-Jul-2012 |
出版者: | Oxford University Press |
誌名: | International immunology |
巻: | 24 |
号: | 9 |
開始ページ: | 573 |
終了ページ: | 581 |
抄録: | Interferon regulatory factor (IRF)-2 is a transcription factor involved in type I (IFN- α/β) signaling. It has been reported that IRF-2 deficiency results in various immune dysfunctions. However, the role of IRF-2 in B-cell functions needs to be elucidated. Unlike wild-type (WT) B cells, IRF-2(-/-) B2 cells were refractory to anti-IgM, but not LPS. Such a defect in proliferation was dependent on IFN- α/β receptor (IFNAR). Marginal zone B cells increased in the proportion relative to B2 cells in IRF-2(-/-) mice produced IgM normally to LPS stimulation. However, IRF-2(-/-) B2 cells were defective in IgM production in an IFNAR-independent manner, although both B-cell subsets differentiated phenotypically to plasma cells at elevated efficiencies. Class switch recombination of IRF-2(-/-) B2 cells by LPS plus IL-4 was also impaired. Their reduced IgM production was conceivably due to an inefficient up-regulation of Blimp-1. Consistent with these in vitro observations, specific antibody production in vivo to a T-dependent antigen by B2 cells was severely impaired in IRF-2(-/- )mice. However, a low, but significant, level of IgG was detected at a late time point, and this IgG exhibited comparable binding affinity to that in WT mice. Follicular helper T-cell development and germinal center formation were normal. A similar tendency was observed when µ chain(-/-) mice were reconstituted with IRF-2(-/- )B cells. These results revealed a multi-faceted role of IRF-2 in the function of B cells, particularly B2 cells, through regulating proliferation in an IFNAR-dependent manner and antibody production via up-regulation of Blimp-1. |
著作権等: | © The Author 2012. Published by Oxford University Press. この論文は出版社版でありません。引用の際には出版社版をご確認ご利用ください。 This is not the published version. Please cite only the published version. |
URI: | http://hdl.handle.net/2433/176343 |
DOI(出版社版): | 10.1093/intimm/dxs060 |
PubMed ID: | 22773153 |
出現コレクション: | 学術雑誌掲載論文等 |
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