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The tyrosine kinase Syk has been implicated as a key signal transducer from the B cell antigen receptor (BCR). We show here that mutation of the Syk gene completely blocks the maturation of immature B cells into recirculating cells and stops their entry into B cell follicles. Furthermore, using radiation chimeras we demonstrate that this developmental block is due to the absence of Syk in the B cells themselves. Syk-deficient B cells are shown to have the life span of normal immature B cells. If this is extended by over-expression of Bcl-2, they accumulate in the T zone and red pulp of the spleen in increased numbers, but still fail to mature to become recirculating follicular B cells. Despite this defect in maturation, Syk-deficient B cells were seen to give rise to switched as well as nonswitched splenic plasma cells. Normally only a proportion of immature B cells is recruited into the recirculating pool. Our results suggest that Syk transduces a BCR signal that is absolutely required for the positive selection of immature B cells into the recirculating B cell pool.


Journal article


J Exp Med

Publication Date





2013 - 2021


Animals, B-Lymphocytes, Bone Marrow Cells, Cell Differentiation, Cell Separation, Enzyme Precursors, Flow Cytometry, Fluorescent Antibody Technique, Indirect, Intracellular Signaling Peptides and Proteins, Liver, Mice, Mice, Transgenic, Protein-Tyrosine Kinases, Proto-Oncogene Proteins c-bcl-2, Receptors, Antigen, B-Cell, Signal Transduction, Spleen, Syk Kinase