CD45 links the B cell receptor with cell survival and is required for the persistence of germinal centers
Details
Publication Year 2006-02, Volume 7, Issue #2, Page 190-198
Journal Title
NATURE IMMUNOLOGY
Publication Type
Journal Article
Abstract
To segregate the many contributions that B cell receptor (BCR)-mediated signals make to immune responses, we have analyzed here B cells deficient in the 'pan-leukocyte' marker CD45. BCR ligation of Cd45(-/-) B cells failed to activate phosphatidylinositol-3-OH kinase, NF-kappa B, Erk1 or Erk2 kinases or to upregulate cell survival proteins and instead induced apoptosis. Immunization of Cd45(-/-) B cell chimeras induced germinal centers and antigen-specific immunoglobulin G1 antibody-forming cells early, but both cellular compartments decreased by day 14. Proliferation of Cd45(-/-) B cells induced by CD40 ligand in vitro was impaired as a result of abrogation by BCR ligation of the upregulation of prosurvival proteins. In contrast, enforced expression of the antiapoptotic factor Bcl-x(L) prevented the collapse of Cd45(-/-) B cell germinal centers. These results show mechanistic differences in B cell survival during germinal center initiation and propagation; CD40 signaling is sufficient for the former, whereas the latter requires signaling from the BCR.
Publisher
NATURE PUBLISHING GROUP
Keywords
PHOSPHATASE-DEFICIENT MICE; T-CELL; SOMATIC HYPERMUTATION; IMMUNE-RESPONSE; MOLECULAR CHARACTERIZATION; LYMPHOCYTE DEVELOPMENT; CD45-DEFICIENT MICE; TRANSGENIC MICE; SELECTION; MEMORY
Publisher's Version
https://doi.org/10.1038/ni1292
Rights Notice
Refer to copyright notice on published article.


Creation Date: 2006-02-01 12:00:00
Last Modified: 0001-01-01 12:00:00
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