摘要
研究SP对NK92-MI细胞杀伤活性以及活化性受体NCRs(NKp46、NKp44和NKp30分子)的表达的影响,揭示SP对NK细胞杀伤功能的调节作用及其内在作用机制。MTT法测定NK92-MI细胞对K562细胞的杀伤活性;Real-Time PCR检测NCRs的mRNA表达;流式细胞术检测NCRs的膜表达。在10-14~10-8mol/L浓度范围的SP作用24 h,对NK92-MI细胞的杀伤活性有明显增强作用;10-14~10-8mol/L的SP,均可增加NK92-MI细胞活化性受体NKp44、NKp46及NKp30的mRNA表达;该浓度范围的SP均可增加NKp46的膜表达水平,仅较低浓度(10-14mol/L)的SP对NKp44的膜表达水平有增加作用,各浓度的SP对NKp30的膜表达水平均无明显影响。SP可通过上调活化性受体NCRs的表达水平来调节NK细胞的活性。
The effects on eytotoxieity and expression of cell activation receptors NCRs (NKp46 ,NKp44 and NKp30) in NK92-MI cells by substance P (SP) were studied to reveal the mechanism of regulating NK cell activity and its inherent effective mechanism by SP. MTT assay was used to detect NK92-MI cell cytotoxieity; Real-Time PCR was used for detecting mRNA expression of NCRs; Using Flow cytometry to analyze membrane expression of NCRs. The results showed that SP at concentration of 10^-14 - 10^-8 mol/L treated for 24 h significantly enhanced the cytotoxicity of NK92-MI cell; SP at concentrations of 10^-14 - 10^-8 mol/L could increase all and significantly the expression of cell activation receptors NKp44, NKp46, and NKp30 mRNA in NK92-MI cells. In cells treated with SP at the concentration range, the membrane expression of NKp46 could significantly increase. Only a fairly low SP concentration ( 10 ^-14 mol/L) had increasing effect on membrane expression of NKp44. However, various SP concentrations had no significant effect on membrane expression of NKp30. Therefore, SP could regulate NK cell activities through up-regulating the expression of activated receptor NCRs.
出处
《微生物学杂志》
CAS
CSCD
2012年第1期64-69,共6页
Journal of Microbiology