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CD19 differentially regulates BCR signalling through the recruitment of PI3K
journal contributionposted on 2023-05-20, 06:57 authored by Xu, Y, Kirsten FairfaxKirsten Fairfax, Light, A, Huntington, ND, Tarlinton, DM
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.
Department/SchoolMenzies Institute for Medical Research
PublisherTaylor & Francis Ltd
Place of publication4 Park Square, Milton Park, Abingdon, England, Oxon, Ox14 4Rn
Rights statementCopyright 2014 Informa UK Ltd.