Appleby M W, Kerner J D, Chien S, Maliszewski C R, Bondada S, Perlmutter R M, Bondadaa S [corrected to Bondada S ]
Howard Hughes Medical Institute, Seattle, Washington 98195, USA.
J Exp Med. 1995 Sep 1;182(3):811-20. doi: 10.1084/jem.182.3.811.
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.
先前的研究表明，非受体蛋白酪氨酸激酶（PTK）p59fyn参与了B细胞抗原受体信号的传导。为了阐明这种激酶的功能，我们检测了经基因工程改造而缺乏p59fyn造血异构体的小鼠的B细胞反应性。值得注意的是，抗原受体信号传导在fynT基因敲除的B细胞中仅有轻微缺陷。相比之下，白细胞介素（IL）-5受体的信号传导（该信号传导通常与抗免疫球蛋白一起提供协同刺激）则被完全阻断。我们的结果证明了p59fynT在B细胞IL-5反应中的重要性，并且支持了一种涉及至少同时募集三个PTK家族的细胞因子受体信号转导的通用模型。
