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Survival of Igɑ-Deficient Mature B Cells Requires BAFF-R Function

MPS-Authors

Levit-Zerdoun,  Ella
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Becker,  Martin
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Pohlmeyer,  Roland
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Maity,  Palash Chandra
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Reth,  Michael
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Hobeika,  Elias
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Citation

Levit-Zerdoun, E., Becker, M., Pohlmeyer, R., Wilhelm, I., Maity, P. C., Rajewsky, K., et al. (2016). Survival of Igɑ-Deficient Mature B Cells Requires BAFF-R Function. The Journal of Immunology, 196, 2348-2360. doi:10.4049/jimmunol.1501707.


Cite as: http://hdl.handle.net/11858/00-001M-0000-002C-AF99-D
Abstract
Expression of a functional BCR is essential for the development of mature B cells and has been invoked in the control of their maintenance. To test this maintenance function in a new experimental setting, we used the tamoxifen-inducible mb1-CreERT2 mouse strain to delete or truncate either the mb-1 gene encoding the BCR signaling subunit Igα or the VDJ segment of the IgH (H chain [HC]). In this system, Cre-mediated deletion of the mb-1 gene is accompanied by expression of a GFP reporter. We found that, although the Igα-deficient mature B cells survive for >20 d in vivo, the HC-deficient or Igα tail-truncated B cell population is short-lived, with the HC-deficient cells displaying signs of an unfolded protein response. We also show that Igα-deficient B cells still respond to the prosurvival factor BAFF in culture and require BAFF-R signaling for their in vivo maintenance. These results suggest that, under certain conditions, the loss of the BCR can be tolerated by mature B cells for some time, whereas HC-deficient B cells, potentially generated by aberrant somatic mutations in the germinal center, are rapidly eliminated.