Normal B-1 cell development but defective BCR signaling in LCK–/– mice

✍ Scribed by Cristina Ulivieri; Silvia Valensin; M. Bernardetta Majolini; R. James Matthews; Cosima T. Baldari

• Book ID: 102279327
• Publisher: John Wiley and Sons
• Year: 2003
• Tongue: English
• Weight: 168 KB
• Volume: 33
• Category: Article
• ISSN: 0014-2980
• DOI: 10.1002/immu.200310019

✦ Synopsis

Abstract

Mature B cells are grouped into two major subsets, B‐1 and B‐2, believed to derive from separate lineages. We have recently shown that B‐1 cells, which are characterized by CD5 surface expression, specifically exhibit significant levels of the tyrosine kinase Lck in man. Here we show that also in mice Lck expression is restricted to B‐1 cells and address the potential role of Lck in B‐1 cell development and activation. Using as a model an Lck^–/–^ mouse, we show that, while dispensable for B‐1 cell development, Lck is required for full and sustained activation of the tyrosine phosphorylation and MAP kinase cascades triggered by the BCR in CD5^+^, B‐1 cells. The data suggest a potential role for Lck in the achievement of the higher activation threshold required for productive BCR signaling in B‐1 as compared to B‐2 cells.