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Survival of Igα-deficient mature B cells requires BAFF-R function

Item Type:Article
Title:Survival of Igα-deficient mature B cells requires BAFF-R function
Creators Name:Levit-Zerdoun, E. and Becker, M. and Pohlmeyer, R. and Wilhelm, I. and Maity, P.C. and Rajewsky, K. and Reth, M. and Hobeika, E.
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 Igalpha 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 Igalpha-deficient mature B cells survive for >20 d in vivo, the HC-deficient or Igalpha tail-truncated B cell population is short-lived, with the HC-deficient cells displaying signs of an unfolded protein response. We also show that Igalpha-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.
Keywords:B-Cell Activation Factor Receptor, B-Lymphocytes, Cell Survival, Endoplasmic Reticulum Stress, Gene Expression, Knockout Mice, Phenotype, Protein Interaction Domains and Motifs, Sequence Deletion, Signal Transduction, Transgenic Mice, Animals, Mice
Source:Journal of Immunology
Publisher:American Association of Immunologists
Page Range:2348-2360
Date:1 March 2016
Official Publication:https://doi.org/10.4049/jimmunol.1501707
PubMed:View item in PubMed

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