Abstract
Mutations in Bruton's tyrosine kinase (Btk) result in the B cell immunodeficiencies XLA in humans and Xid in mice. Both the maintenance of peripheral B cell numbers and their response to B cell antigen receptor (BCR) crosslinking de"- pend on Btk. Btk integrates signals from multiple cell surface recep tors, including BCR and G-protein coupled receptors. These Btk dependent signals control B cell prolifer"- ation and survival by mediating Ca2+flux, activating JNK and p38 and inducing cell cycle regulatory genes.
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