Abstract
CD5 is a membrane protein that is homologous to the scavenger receptor family of macrophages. The cytoplasmic domain of CD5 contains tyrosine residues that are inducibly phosphorylated in T-cells, but are constitutively phosphorylated in B-1 cells. This chapter presents a study in which CD5–/– mice had an apparently healthy phenotype. Numbers of T and B lymphocytes, both of which lacked CD5 expression, were found to be similar to those in control mice. Near-normal immune responses to T cell-dependent and T cell-independent antigens were exhibited. Thymocytes from CD5–/– mice were found to be hyper-responsive to stimulation through the TCR in vitro, and thymic selection of transgenic T cells was impaired. Studies in vitro showed that B-1 cells from CD5-deflcient mice did not exhibit a particular B cell receptor (BCR) signalling defect seen in control mice: B-1 cells from CD5–/–, but not control mice, proliferated in response to stimulation with anti-IgM antibodies. B-1 cells from control mice, but not CD5–/– mice, underwent apoptosis in response to BCR-mediated signaling. These differences in growth responses appeared to be due to changes in early signaling events induced by BCR crosslinking. Thus, calcium mobilization appeared to be more sustained in CD5–/– B-1 cells than in control cells. The results indicate that the CD5 antigen is encoded by the same gene in both B and T cells.
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