摘要
为研究NK细胞表面分子在NK细胞激活及释放细胞因子中的作用及其机制,作者用系列粘附分子单抗、配体及基因转染细胞刺激或共刺激NK细胞,定量检测IFN-γ的分泌。结果表明,CD45分子交联可独立激活NK细胞,CD45分子的信号传递作用对CD16分子无依赖性。随着NK细胞的成熟与分化,其表面CD45分子的表达呈现RA向RO变化的特征,而RO的交联,对NK细胞的刺激显著强于RA的交联。CD22α和CD22β基因转染细胞能显著粘附NK细胞系NK3.3(RO^+),但并不能有效刺激其产生IFN-γ。作者推测,CD45分子,尤其是CD45RO,是NK细胞表面独特的信号传递分子,通过直接激活Src家族的PTK成员,开启独立的、非CD16分子参与的NK细胞内信号传递途径。
For identifying the molecules that trigger NK cell activation and investigating the mechanism by which the identified molecule mediates NK cell signal transduction, NK cells was stimulated with mAbs specific for a series of adhesion molecules their ligands and transfectants. IFN-gamma production by NK cells was quantitated. We first report here that crosslinking of CD45 specifically stimulates INF-gamma production in NK cells, and such effect was independent of CD16. NK cells gradually lose expression of CD45RA upon culture with IL-2 and concomitantly acquire the expression of CD45RO. CD45RO, rather than CD45RA, play stimulating roles in INF-gamma production in NK cells. Whereas NK cells bound to CD22α and CD22β transfectants, this interaction was not able to stimulate NK cells to secrete IFN - gamma. Our observation suggests that CD45 crosslinking, as an independent and unique stimuli, mediates NK cell signaling.
出处
《中国肿瘤生物治疗杂志》
CAS
CSCD
1996年第1期6-10,5,共6页
Chinese Journal of Cancer Biotherapy
