摘要
选择NK92-MI细胞为研究体系,研究SP对NK细胞的杀伤活性及功能性受体NKG2D/NKG2A表达的影响,以探讨SP对NK细胞功能的调节作用机制。采用MTT法测定NK92-MI细胞对K562细胞的杀伤活性;采用Real-Time PCR和流式细胞术检测NK92-MI细胞活化性受体NKG2D和抑制性受体NKG2A的基因表达和膜表达。10-14~10-8 mol/L的SP在体外可明显增强NK92-MI细胞的杀伤活性。该浓度范围的SP均可上调NKG2D/NKG2A的mRNA水平;10-14~10-8 mol/L的SP均上调NKG2D/NKG2A的膜表达,较低浓度(10-14 mol/L)的SP仅使NKG2D表达上调,而NKG2A表达无明显变化;SP刺激NKG2D膜表达增加的程度高于NKG2A。生物肽SP调节NK细胞功能性受体NKG2D/NKG2A的表达,可能是SP增强NK细胞杀伤活性的一种原因。
NK92-MI cell was selected as a research system to study the effects of substance P (SP) on killing activity and functional receptor of the expression of NKG2D/NKG2A in order to study the regulation mechanism of SP on NK cellular functions. MTT assay was used to detect NK92-MI cell killing activity against K562 cell, and Real-Time PCR and FACS were used to detect gene expression and membrane expression of NK92-MI cell activated receptor NKG2D and inhibitory receptor NKG2A. The results showed that 1. SP in vitro at concentration of 10 -,4 - 10 -5mol/L, could remarkably enhance the killing activity of NK92-MI cells. The concentration range of SP could up-regulated the mRNA level; 10-14- 10-5 mol/L of SP up-regulated membrane expression of NKG2D/NKG2A; while lower concentration ( 10 -t4 tool/L) up-regulated only the expression of NKG2D, but not remarkable change on the expression of NKG2A. The increment degree of NKG2D membrane expression stimulated by SP was higher than NKG2A. Therefore, the expression of NK cell functional receptor NKG2D/NKG2A regulated by bio-peptide SP was possibly one of the reasons that SP strengthened the killing activity of NK cell.
出处
《微生物学杂志》
CAS
CSCD
2011年第6期57-61,共5页
Journal of Microbiology