Cookies on this website
We use cookies to ensure that we give you the best experience on our website. If you click 'Continue' we'll assume that you are happy to receive all cookies and you won't see this message again. Click 'Find out more' for information on how to change your cookie settings.

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.

Type

Journal article

Journal

J Exp Med

Publication Date

15/12/1997

Volume

186

Pages

2013 - 2021

Keywords

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