Syk-deficient eosinophils show normal interleukin-5-mediated differentiation, maturation, and survival but no longer respond to FcgammaR activation.
Syk-deficient eosinophils show normal interleukin-5-mediated differentiation, maturation, and survival but no longer respond to FcgammaR activation.
复制标题
Syk 缺陷的嗜酸性粒细胞表现出正常的白细胞介素 5 介导的分化、成熟和存活,但不再对 FcgammaR 激活做出反应。
作者:
E. Lach‐Trifilieff;K. Menear;E. Schweighoffer;V. Tybulewicz;C. Walker
The tyrosine kinase Syk has been proposed to play a critical role in the antiapoptotic effect of interleukin (IL)-5 in human eosinophils. However, little is known about the involvement of Syk in other IL-5-mediated activation events. To further address these questions, the role of Syk in IL-5-induced eosinophil differentiation, activation, and survival was analyzed using cells obtained from Syk-deficient mice. We could demonstrate that Syk-deficient fetal liver cells differentiate into mature eosinophils in response to IL-5 at the same rate as wild-type fetal liver cells and generate the same total number of eosinophils. Moreover, no difference in IL-5-induced survival of mature eosinophils between Syk(-/-) and wild-type eosinophils could be demonstrated, suggesting that the antiapoptotic effect of IL-5 does not require Syk despite the activation of this tyrosine kinase upon IL-5 receptor ligation. In contrast, eosinophils derived from Syk-deficient but not wild-type mice were incapable of generating reactive oxygen intermediates in response to Fcgamma receptor (FcgammaR) engagement. Taken together, these data clearly demonstrate no critical role for Syk in IL-5-mediated eosinophil differentiation or survival but underline the importance of this tyrosine kinase in activation events induced by FcgammaR stimulation.
DOI:
10.1073/pnas.93.18.9704
发表时间:
1996-09-03
影响因子:
11.1
作者:
MallickWood, CA;Pao, W;Hayday, AC
通讯作者:
Hayday, AC
影响因子:
14.2
作者:
GLEICH, GJ
通讯作者:
GLEICH, GJ
DOI:
10.1126/science.3110954
发表时间:
1987
期刊:
Science (New York, N.Y.)
影响因子:
--
作者:
Rothenberg,ME;OwenJr,WF;Silberstein,DS;Soberman,RJ;Austen,KF;Stevens,RL
通讯作者:
Stevens,RL