期刊
JOURNAL OF IMMUNOLOGY
卷 196, 期 5, 页码 2348-2360出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1501707
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资金
- Deutsche Forschungsgemeinschaft [SFB746, TRR130, EXC294, SFB 1074]
- European Research Council Grant [322972, 268921]
- Excellence Initiative of the German Research Foundation (Spemann Graduate School) [GSC-4]
- European Research Council (ERC) [322972, 268921] Funding Source: European Research Council (ERC)
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 Ig alpha 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 Ig alpha-deficient mature B cells survive for >20 d in vivo, the HC-deficient or Iga tail-truncated B cell population is short-lived, with the HC-deficient cells displaying signs of an unfolded protein response. We also show that Iga-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.
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