INVOLVEMENT OF P59FYN(T) IN INTERLEUKIN-5 RECEPTOR SIGNALING

Previous studies implicate the nonreceptor protein tyrosine kinase (PTK) p59(fyn) in the propagation of signals from the B cell antigen receptor. To elucidate the functions of this kinase, we examined B cell responsiveness in mice engineered to lack the hematopoietic isoform of p59(fyn). Remarkably, antigen receptor signaling was only modestly defective in fyn(Tnull) B cells. In contrast, signaling from the interleukin (IL)-5 receptor, which ordinarily provides a comitogenic stimulus with antiimmunoglobulin, was completely blocked. Our results document the importance of p59(fynT) in IL-5 responses in B cells, and they support a general model for cytokine receptor signal transduction involving the simultaneous recruitment of at least three families of PTK.