NDLI: c-Abl-deficient mice exhibit reduced numbers of peritoneal B-1 cells and defects in BCR-induced B cell activation

Content Provider	PubMed Central
Author	Liberatore, Rachel A. Goff, Stephen P.
Copyright Year	2009
Abstract	A role for c-Abl in B cell development and signaling has been suggested by previous work showing that c-Abl-deficient mice have defects in bone marrow B cell development and that c-Abl-deficient B cells are hypoproliferative in response to antigen receptor stimulation. Here we show that in addition to defects in early B cell development, c-Abl-deficient mice have defects in peripheral B cell development, including reduced percentages of peritoneal B-1 cells as well as transitional and marginal zone B cells in the spleen. It has been shown that c-Abl kinase activity increases upon B cell receptor (BCR) stimulation and that one of the targets of tyrosine phosphorylation by c-Abl is CD19. However, the consequences of c-Abl activity on B cell activation and CD19 signaling remain unknown. Here, we show that c-Abl-deficient splenic B cells exhibit reduced calcium flux in response to CD19 cross-linking, consistent with a role for c-Abl in CD19-dependent signaling. Additionally, we show that c-Abl-deficient B cells are defective in their ability to be activated in response to antigen receptor engagement, suggesting a functional role for c-Abl in BCR-dependent activation signaling pathways.
Related Links	http://dx.doi.org/10.1093/intimm/dxp006
Ending Page	414
Page Count	12
Starting Page	403
File Format	PDF
ISSN	09538178
e-ISSN	14602377
Journal	International Immunology
Issue Number	4
Volume Number	21
Language	English
Publisher	Oxford University Press
Publisher Date	2009-04-01
Access Restriction	Open
Rights Holder	Oxford University Press
Subject Keyword	Immunology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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