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

被引：60
作者：
APPLEBY, MW
KERNER, JD
CHIEN, S
MALISZEWSKI, CR
BONDADAA, S
PERLMUTTER, RM
机构：
[1] UNIV WASHINGTON, HOWARD HUGHES MED INST, SEATTLE, WA 98195 USA
[2] UNIV WASHINGTON, DEPT IMMUNOL, SEATTLE, WA 98195 USA
[3] UNIV WASHINGTON, DEPT BIOCHEM, SEATTLE, WA 98195 USA
[4] UNIV WASHINGTON, DEPT MED MED GENET, SEATTLE, WA 98195 USA
[5] IMMUNEX RES & DEV CORP, DEPT IMMUNOL, SEATTLE, WA 98101 USA
[6] UNIV KENTUCKY, DEPT MICROBIOL & IMMUNOL, LEXINGTON, KY 40536 USA
来源：
JOURNAL OF EXPERIMENTAL MEDICINE | 1995年 / 182卷 / 03期
关键词：
D O I：
10.1084/jem.182.3.811
中图分类号：
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号：
100102 ;
摘要：
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.
引用
收藏
页码：811 / 820
页数：10
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