CD19 differentially regulates BCR signalling through the recruitment of PI3K
Details
Publication Year 2014, Volume 47, Issue #7, Page 430-437
Journal Title
Autoimmunity
Publication Type
Journal Article
Abstract
Abstract CD19 is a co-stimulatory surface protein expressed exclusively on B cells and serves to reduce the threshold for signalling via the B-cell receptor (BCR). Co-ligation of CD19 with the BCR synergistically enhances mitogen-activated protein (MAP) kinase activity, calcium release and proliferation. We recently found that these parameters were also enhanced in CD19-null primary murine B cells following BCR ligation, suggesting a regulatory role for CD19 in BCR signalling. In this study, we demonstrate that the enhanced BCR signalling in the absence of CD19 was not dependent on the src kinase Lyn, but linked to phosphoinositide 3-kinase (PI3K) activity. Consistent with this, we detect PI3K associated with CD19 outside the lipid raft in resting B cells. Pre-ligation of CD19 to restrict its translocation with the BCR into lipid rafts attenuated BCR-induced PI3K and MAP kinase activation and subsequent B-cell proliferation. Thus, we propose that CD19 can modulate BCR signalling in both a positive and negative manner depending on the receptor/ligand interaction in vivo.
Publisher
Informa
WEHI Research Division(s)
Immunology; Molecular Medicine; Molecular Immunology
PubMed ID
24953501
Rights Notice
Refer to copyright notice on published article.


Creation Date: 2014-07-29 03:01:16
Last Modified: 2016-01-12 12:50:46
An error has occurred. This application may no longer respond until reloaded. Reload 🗙