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| Item Type: | Article |
|---|---|
| Title: | Survival of Igα-deficient mature B cells requires BAFF-R function |
| Creators Name: | Levit-Zerdoun, E., Becker, M., Pohlmeyer, R., Wilhelm, I., Maity, P.C., Rajewsky, K., 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 |
| ISSN: | 0022-1767 |
| Publisher: | American Association of Immunologists |
| Volume: | 196 |
| Number: | 5 |
| 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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