Cutting Edge: B Cell Linker Protein Is Dispensable for the Allelic Exclusion of Immunoglobulin Heavy Chain Locus But Required for the Persistence of CD5+ B Cells

Abstract

The pre-B cell receptor (pre-BCR) and the BCR are required for B lymphopoiesis and for the allelic exclusion of Ig genes. Mice lacking B cell linker (BLNK) protein that is a component of the BCR signaling pathway have impaired B cell development. In this report, we show that allelic exclusion is intact in BLNK−/− mice harboring a VH12 transgene. This differs from mice lacking the tyrosine kinase Syk that is upstream of BLNK in BCR signaling and contrasts with mice lacking SLP-76 that is the equivalent adaptor molecule in TCR-signal transduction. We also show that, whereas most wild-type VH12-expressing B cells are CD5+, the majority of the splenic VH12-expressing BLNK−/− B cells are CD5−. A small population of VH12-expressing, BLNK−/− CD5+ B cells is detectable in the peritoneal cavity of younger but not older mice. This suggests that BLNK deficiency affects not only the generation but also the persistence of B-1 cells.