Involvement of p59fynT in interleukin-5 receptor signaling [published erratum appears in J Exp Med 1995 Oct 1;182(4):1179]

doi:10.1084/jem.182.3.811

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Involvement of p59fynT in interleukin-5 receptor signaling [published erratum appears in J Exp Med 1995 Oct 1;182(4):1179]

MW Appleby, JD Kerner, S Chien, CR Maliszewski, S Bondada, RM Perlmutter and S] Bondadaa S [corrected to Bondada
Howard Hughes Medical Institute, Seattle, Washington 98195, USA.

Previous studies implicate the nonreceptor protein tyrosine kinase (PTK) p59fyn 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 p59fyn. Remarkably, antigen receptor signaling was only modestly defective in fynTnull 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 p59fynT 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.
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