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J Immunol. 2016 Mar 1;196(5):2348-60. doi: 10.4049/jimmunol.1501707. Epub 2016 Feb 3.

Survival of Igα-Deficient Mature B Cells Requires BAFF-R Function.

Author information

1
Max Planck Institute of Immunobiology and Epigenetics, 79108 Freiburg, Germany; Department of Molecular Immunology, Biology III, Faculty of Biology, Albert-Ludwigs-University Freiburg, 79104 Freiburg, Germany; International Max Planck Research School for Molecular and Cellular Biology, 79108 Freiburg, Germany;
2
Max Planck Institute of Immunobiology and Epigenetics, 79108 Freiburg, Germany; Department of Molecular Immunology, Biology III, Faculty of Biology, Albert-Ludwigs-University Freiburg, 79104 Freiburg, Germany; Centre for Biological Signaling Studies, University of Freiburg, 79104 Freiburg, Germany;
3
Department of Molecular Immunology, Biology III, Faculty of Biology, Albert-Ludwigs-University Freiburg, 79104 Freiburg, Germany; Centre for Biological Signaling Studies, University of Freiburg, 79104 Freiburg, Germany; Spemann Graduate School of Biology and Medicine, Albert-Ludwigs-University Freiburg, 79104 Freiburg, Germany;
4
Max Delbrück Center for Molecular Medicine, 13125 Berlin, Germany; and.
5
Max Planck Institute of Immunobiology and Epigenetics, 79108 Freiburg, Germany; Department of Molecular Immunology, Biology III, Faculty of Biology, Albert-Ludwigs-University Freiburg, 79104 Freiburg, Germany; Centre for Biological Signaling Studies, University of Freiburg, 79104 Freiburg, Germany; michael.reth@bioss.uni-freiburg.de elias.hobeika@uni-ulm.de.
6
Max Planck Institute of Immunobiology and Epigenetics, 79108 Freiburg, Germany; Centre for Biological Signaling Studies, University of Freiburg, 79104 Freiburg, Germany; Institute of Immunology, University Hospital Ulm, 89081 Ulm, Germany michael.reth@bioss.uni-freiburg.de elias.hobeika@uni-ulm.de.

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-CreER(T2) 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.

PMID:
26843325
DOI:
10.4049/jimmunol.1501707
[Indexed for MEDLINE]
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