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生物肽SP对NK细胞NKG2D/NKG2A受体表达的影响 被引量:2

Effects of Bio-Peptide SP on the Expression of NK Cells NKG2AD/NK922A Receptor
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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
关键词 P物质 NK92-MI细胞 杀伤活性 NKG2A NKG2D substance P NK92-MI cell killing activity NKG2A NKG2D
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参考文献12

  • 1Koon HW,Pothoulakis C.Immunomodulatory properties of substance P:the gastrointestinal system as a model[J].Ann N Y Acad Sci,2006,1088:23-40.
  • 2Yasphal K,Wright DM,Henry JL.Substance P reduced tailflick latency:implications for chronic pain syndrome[J].Pain,1982,14(2):155-167.
  • 3Katsanos GS,Anogeianaki A,Orso C,et al.Impact of substance P on cellular immunity[J].J Biol Regul Homeost Agents,2008,22 (2):93-98.
  • 4Steven D.Douglas and Susan E.Leeman.Neurokinin-1 receptor:functional significance in the immune system in reference to selected infections and inflammation[J].Ann.N.Y.Acad.Sci,2011,1217:83-95.
  • 5Fu WX,Qin B,Zhou AP,et al.Regulation of NK92-MI Cell Cytotoxicity by Substance P.Scandinavian Journal of Immunology[J].Scand J Immunol,2011,74(2):107-113.
  • 6Kulka M,Sheen CH,Tancowny BP,et al.Neuropeptides activate human mast cell degranulation and chemokine production[J].Immunology,2008,23 (3):398-410.
  • 7Carina Strell,Anne Sievers,Philipp Bastian,et al.Divergent effects of norepinephrine,dopamine and substance P on the activation,differentiation and effector functions of human cytotoxic T lymphocytes[J].BMC Immunology,2009,10:62-76.
  • 8Lighvani S,Huang X,Trivedi PP,et al.Substance P regulates natural killer cell interferon-γ production and resistance to Pseudomonas aeruginosa infection[J].Eur J.Immunol,2005,35 (5):1567-1575.
  • 9Feistritzer C,Clausen J,Sturn DH.et al.Natural killer cell function mediated by the neuropeptide substance P[J].Regulatory Peptidas,2003,116(1-3):119-126.
  • 10Marras F,Bozzano F,De Maria A.Involvement of Activating NK Cell Receptors and Their Modulation Pathogen Immunity[J].J Biomed Biotechnol,2011,2011:152430.Epub.

同被引文献13

  • 1Lagadari M,Lehmann K,Ziemer M. Sphingosine-1-phosphate inhibits the cytotoxic activity of NK cells via Gs protein-mediated signalling[J].International Journal of Oncology,2009,(01):287-294.
  • 2Fu WX,Qin B,Zhou AP,et ai. Regulation of NK92-MI cell cytotoxicity by substance P[J].Scandinavian Journal of Immunology,2011,(02):107-113.
  • 3Ulfers AL,Piserchio A,Mierke DF. Extracellular domains of the neurokinin-1 receptor:structural characterization and interactions with substance P[J].Biopolymers(Peptide Science),2002,(05):339-349.
  • 4Bradley J,McLoughlin D. Use of the DiscoveRx Hit hunter cAMPII assay for direct measurement of cAMP inGs and Gi GPCRs[J].Methods in Molecular Biology,2009.171-179.
  • 5Hohenegger M,Waldhoer M,Beindl W. Gsalpha-selectire G protein antagonists[J].Proceedings of the National Academy of Sciences(USA),1998,(01):346-351.
  • 6Wang R,Jaw JJ,Stutzman NC. Natural killer cell-produced IFN-γ and TNF-α induce target cell cytolysis through upregulation of ICAM-1[J].Journal of Leukocyte Biology,2012,(02):299-309.
  • 7Korbel DS,Finney OC,Riley EM. Natural killer cells and innate immunity to protozoan pathogens[J].International Journal for Parasitology,2004,(13-14):1517-1528.
  • 8Theorell J,Schlums H,Chiang SC. Sensitive and viable quantification of inside-out signals for LFA-1 activation in human cytotoxic iymphocytes by flow cytometry[J].Journal of Immunological Methods,2011,(1-2):106-118.
  • 9傅炜昕,秦博,顾鹏毅,黄勤俊,梁再赋.生物肽SP对NK细胞活化性受体NCRs表达的影响[J].微生物学杂志,2012,32(1):64-69. 被引量:1
  • 10黄可,刘日阳.传染性单核细胞增多症患儿血淋巴细胞亚群变化的意义[J].实用医学杂志,2012,28(11):1867-1869. 被引量:11

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