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Title: Mitochondrial function provides instructive signals for activation-induced B-cell fates.
Authors: Jang, Kyoung-Jin
Mano, Hiroto
Aoki, Koji
Hayashi, Tatsunari
Muto, Akihiko
Nambu, Yukiko
Takahashi, Katsu  kyouindb  KAKEN_id
Itoh, Katsuhiko  kyouindb  KAKEN_id
Taketani, Shigeru
Nutt, Stephen L
Igarashi, Kazuhiko
Shimizu, Akira  kyouindb  KAKEN_id
Sugai, Manabu
Author's alias: ジャン, キョンジン
青木, 耕史
竹谷, 茂
五十嵐, 和彦
清水, 章
菅井, 学
Keywords: Biological sciences
Issue Date: 10-Apr-2015
Publisher: Nature Publishing Group
Journal title: Nature communications
Volume: 6
Thesis number: 6750
Abstract: During immune reactions, functionally distinct B-cell subsets are generated by stochastic processes, including class-switch recombination (CSR) and plasma cell differentiation (PCD). In this study, we show a strong association between individual B-cell fates and mitochondrial functions. CSR occurs specifically in activated B cells with increased mitochondrial mass and membrane potential, which augment mitochondrial reactive oxygen species (mROS), whereas PCD occurs in cells with decreased mitochondrial mass and potential. These events are consequences of initial slight changes in mROS in mitochondria(high) B-cell populations. In CSR-committed cells, mROS attenuates haeme synthesis by inhibiting ferrous ion addition to protoporphyrin IX, thereby maintaining Bach2 function. Reduced mROS then promotes PCD by increasing haeme synthesis. In PCD-committed cells, Blimp1 reduces mitochondrial mass, thereby reducing mROS levels. Identifying mROS as a haeme synthesis regulator increases the understanding of mechanisms regulating haeme homeostasis and cell fate determination after B-cell activation.
Description: 機能的抗体産生を制御する活性化B細胞運命決定機構の解明 京都大学プレスリリース. 2015-04-14.
Rights: This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit
DOI(Published Version): 10.1038/ncomms7750
PubMed ID: 25857523
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