Miltenyi Biotec GmbH
Originally published online as doi:10.1189/jlb.0109037 on May 19, 2009

Published online before print May 19, 2009
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(Journal of Leukocyte Biology. 2009;86:205-218.)
© 2009 Society for Leukocyte Biology

Pivotal Advance: CEACAM1 is a negative coreceptor for the B cell receptor and promotes CD19-mediated adhesion of B cells in a PI3K-dependent manner

Elizabeth O. Lobo, Zhifang Zhang and John E. Shively1

Division of Immunology, Beckman Research Institute at City of Hope, Duarte, California, USA

1. Correspondence: Division of Immunology, Beckman Research Institute at City of Hope, Duarte, CA 91010, USA. E-mail: jshively{at}coh.org

ABSTRACT

Upon antigen binding, the BCR transduces a signal culminating in proliferation or in AICD of the B cell. Coreceptor engagement and subsequent modification of the BCR signal pathway are mechanisms that guide the B cell to its appropriate fate. For example, in the absence of coreceptor engagement, anti-sIgM antibodies induce apoptosis in the human Daudi B cell lymphoma cell line. ITIM-bearing B cell coreceptors that potentially may act as negative coreceptors include FcR{gamma}IIb, CD22, CD72, and CEACAM1 (CD66a). Although the role of CEACAM1 as an inhibitory coreceptor in T cells has been established, its role in B cells is poorly defined. We show that anti-sIgM antibody and PI3K inhibitor LY294002-induced apoptosis are reduced significantly in CEACAM1 knock-down clones compared with WT Daudi cells and that anti-sIgM treatment induced CEACAM1 tyrosine phosphorylation and association with SHP-1 in WT cells. In contrast, treatment of WT Daudi cells with anti-CD19 antibodies does not induce apoptosis and has reduced tyrosine phosphorylation and SHP-1 recruitment to CEACAM1. Thus, similar to its function in T cells, CEACAM1 may act as an inhibitory B cell coreceptor, most likely through recruitment of SHP-1 and inhibition of a PI3K-promoted activation pathway. Activation of B cells by anti-sIgM or anti-CD19 antibodies also leads to cell aggregation that is promoted by CEACAM1, also in a PI3K-dependent manner.

Key Words: SHP-1 • apoptosis • activation-induced cell death • cell aggregation


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