Syk deficiency in human non-releaser lung mast cells.
Syk deficiency in human non-releaser lung mast cells.
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人类非释放肺肥大细胞中 Syk 缺陷。
DOI：
10.1016/j.clim.2007.06.006
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发表时间：
2007
期刊：
影响因子：
--
通讯作者：
Kepley,Christopher
中科院分区：
文献类型：
--
作者：
Gomez,Gregorio;Schwartz,Lawrence;Kepley,Christopher
与外周血嗜碱性粒细胞一样，人肺肥大细胞也可能具有非趋化因子表型，其特征为对FcεRI-IgE介导的刺激无应答（1）。先前对人嗜碱性粒细胞的研究表明，约10-15%的供体不能响应FcεRI交联而释放组胺（2-5），酪氨酸激酶Syk蛋白水平降低与这种非组胺释放状态相关（6; 7）。在这里，我们提出的证据减少Syk蛋白在第二次制备的肺肥大细胞与nonreleasing phenotype.Mast细胞分离从废弃的手术肺内获得24小时的手术，由VCU IRB批准。通过切碎肺并用胶原酶和透明质酸酶消化碎片来分散肥大细胞，通过Percoll密度依赖性沉降来富集，并通过使用小鼠IgG抗Kit mAb和珠缀合的抗小鼠Ab的阳性选择来纯化至> 95%纯度。
Human lung mast cells, like peripheral blood basophils, can have a nonreleaser phenotype characterized by a failure to respond to FcεRI-IgE-mediated stimulation (1). Previous studies on human basophils demonstrated that approximately 10–15% of donors fail to release histamine in response to FcεRI crosslinking (2–5) and that depressed protein levels of the tyrosine kinase Syk correlated with this nonreleaser status (6; 7). Here we present evidence for diminished Syk protein in a second preparation of lung mast cells with a nonreleasing phenotype.Mast cells were isolated from discarded surgical lung obtained within 24 h of surgery as approved by the VCU IRB. Mast cells were dispersed by mincing the lung and digesting the pieces with collagenase and hyaluronidase, enriched by Percoll density-dependent sedimentation, and purified to> 95% purity by positive selection using mouse IgG anti-Kit mAb and bead-conjugated anti-mouse Ab.