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CD19 differentially regulates BCR signalling through the recruitment of PI3K


Xu, Y and Fairfax, K and Light, A and Huntington, ND and Tarlinton, DM, CD19 differentially regulates BCR signalling through the recruitment of PI3K, Autoimmunity, 47, (7) pp. 430-437. ISSN 0891-6934 (2014) [Refereed Article]

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Copyright 2014 Informa UK Ltd.

DOI: doi:10.3109/08916934.2014.921810


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.

Item Details

Item Type:Refereed Article
Keywords:B-cell activation, co-receptor, signal transduction
Research Division:Biological Sciences
Research Group:Biochemistry and cell biology
Research Field:Cell development, proliferation and death
Objective Division:Health
Objective Group:Clinical health
Objective Field:Clinical health not elsewhere classified
UTAS Author:Fairfax, K (Dr Kirsten Fairfax)
ID Code:134804
Year Published:2014
Web of Science® Times Cited:11
Deposited By:Menzies Institute for Medical Research
Deposited On:2019-09-05
Last Modified:2019-10-08

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