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Cutting Edge: The Transcription Factor Bob1 Counteracts B Cell Activation and Regulates miR-146a in B cells

MPS-Authors

Lindner,  John M.
Max Planck Society;

Kayo,  Hiroyuki
Max Planck Society;

/persons/resource/persons191089

Hedlund,  Sebastian
Research Group and Chair of Molecular Immunology of the University of Freiburg, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Fukuda,  Yoko
Max Planck Society;

Fukao,  Taro
Max Planck Society;

/persons/resource/persons191248

Nielsen,  Peter J.
Research Group and Chair of Molecular Immunology of the University of Freiburg, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Citation

Lindner, J. M., Kayo, H., Hedlund, S., Fukuda, Y., Fukao, T., & Nielsen, P. J. (2014). Cutting Edge: The Transcription Factor Bob1 Counteracts B Cell Activation and Regulates miR-146a in B cells. The Journal of Immunology, 192, 4483-4486.


Cite as: https://hdl.handle.net/11858/00-001M-0000-002B-8879-5
Abstract
Mice lacking the lymphocyte-specific transcription factor Bob1 (also called OBF-1 or OCA-B) fail to generate germinal centers and a robust Ig response. We show that peripheral B cells in Bob1-/- mice bear characteristics of chronically activated or anergic-like B cells and identify the immunosuppressive microRNA-146a, together with other microRNAs, as novel transcriptional targets of Bob1. The inability to restrict B cell signaling could contribute to the immunodeficient phenotype of these mice and is consistent with an important role for Bob1 in suppressing B cell activation in vivo.