Mitochondrial function provides instructive signals for activation-induced B-cell fates

Kyoung-Jin Jang, Hiroto Mano, Koji Aoki, Tatsunari Hayashi, Akihiko Muto, Yukiko Nambu, Katsu Takahashi, Katsuhiko Itoh, Shigeru Taketani, Stephen L. Nutt, Kazuhiko Igarashi, Akira Shimizu and Manabu Sugai ()
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Kyoung-Jin Jang: Institute for Advancement of Clinical and Translational Science, Kyoto University Hospital
Hiroto Mano: Institute for Advancement of Clinical and Translational Science, Kyoto University Hospital
Koji Aoki: School of Medicine, University of Fukui
Tatsunari Hayashi: Institute for Advancement of Clinical and Translational Science, Kyoto University Hospital
Akihiko Muto: Tohoku University Graduate School of Medicine
Yukiko Nambu: Institute for Advancement of Clinical and Translational Science, Kyoto University Hospital
Katsu Takahashi: Kyoto University Hospital
Katsuhiko Itoh: Graduate School of Medicine, Kyoto University
Shigeru Taketani: Kyoto Institute of Technology
Stephen L. Nutt: The Walter and Eliza Hall Institute of Medical Research
Kazuhiko Igarashi: Tohoku University Graduate School of Medicine
Akira Shimizu: Institute for Advancement of Clinical and Translational Science, Kyoto University Hospital
Manabu Sugai: Institute for Advancement of Clinical and Translational Science, Kyoto University Hospital

Nature Communications, 2015, vol. 6, issue 1, 1-13

Abstract: 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 mitochondriahigh 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.

Date: 2015
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DOI: 10.1038/ncomms7750

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