Sialyl Lewis X binding lectins on natural killer cells and their functions

自然杀伤细胞上唾液酸路易斯X结合凝集素及其功能

基本信息

  • 批准号:
    16590465
  • 负责人:
  • 金额:
    $ 2.18万
  • 依托单位:
  • 依托单位国家:
    日本
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
  • 财政年份:
    2004
  • 资助国家:
    日本
  • 起止时间:
    2004 至 2005
  • 项目状态:
    已结题

项目摘要

Natural killer (NK) cells mediate cytotoxicity through cell-surface receptors including lectin-like receptors. We have investigated whether sialyl Lewis X (sLeX) antigen, Neu5Acα2,3Galβ1,4 (Fucα1,3)GlcNAc-R, can bind to the lectin-like receptor on human NK-derived KHYG cells, using transferrin secreted by human hepatoma-derived HepG2 cells (Hep-TF), whose N-glycans are rich in α1,3-fucosylated bi-, tri-, and tetra-antennary complex types of N-glycans, and commercially available human transferrin (Nor-TF), which is comprised of bi-antennary N-glycans without α1,3-fucosylation.High sLeX-expressing erythroleukemia-derived K562 cells isolated from fucosyltransferase 3-transfected cells were 2.5 fold more susceptible than wild-type K562 cells to KHYG cells. Fluorescein isothiocyanate (FITC)-labeled Hep-TF bound 1.8 fold more strongly to KHYG cells than did FITC-labeled Nor-TF. The binding was suppressed by treatment with anti-NKG2D, anti-NKG2C, anti-CD94, and anti-CD 161 antibodies. FITC-labeled Hep-TF bound more strongly to human monocyte-derived U937 cells transfected with NKG2D and CD94 than to wild-type U937 cells. Moreover, tyrosine phosphorylation of a 17 kDa protein in the KHYG cells was enhanced by incubation on a Hep-TF coated plate and treatment with an anti-NKG2D antibody, but not by a Nor-TF coated plate and an anti-CD94 antibody.These results indicated that the interaction of sLeX antigen with the lectin-like receptors on NK cells induces cytotoxicity, which is mediated through a tyrosine-phosphorylated 17 kDa protein.
天然杀伤(NK)细胞通过包括教授样受体在内的细胞表面受体介导细胞毒性。我们已经研究了siAllyl Lewis X(Slex)抗原,Neu5ACα2,3GALβ1,4(FUCα1,3)GlcNAC-R是否可以使用人类NK衍生的Khhyg细胞上的讲座受体结合,使用人肝瘤的hepG2细胞(hepg2 fried an-fried Bi fribies)的hep-tfucs an-hep-fucs an-fried Bi fried Bi fried HepG2细胞(hep-fucs),其N-fcans and-f in-n-fcans in-n-fcans in-n-fcans。 n-糖果的三 - 和四静脉复杂类型,以及商业上可用的人类转铁蛋白(NOR-TF),由无α1,3-螺旋化的双期n-糖果组成。高表达嗜酸性的erythrololeukia drountythrolookiby farsifed trythroliqused K562细胞均来自富甲基蛋白酶基的iptersylys 3--富含质量均具有3.富含质量的细胞。2. K562细胞到khyg细胞。荧光素异硫氰酸荧光素(FITC)标记的HEP-TF结合1.8倍与khyg细胞的结合比FITC标记的NOR-TF更强烈。通过抗NKG2D,抗NKG2C,抗CD94和抗CD 161抗体的处理来抑制结合。与野生型U937细胞相比,FITC标记的HEP-TF更强烈地与用NKG2D和CD94翻译的人单核细胞衍生的U937细胞结合。此外,通过在HEP-TF涂层板上孵育并用抗NKG2D抗体进行处理,从而增强了Khyg细胞中17 kDa蛋白的酪氨酸磷酸化,从而增强了抗NKG2D抗体,而不是通过NOR-TF涂层的板和抗CD94抗体的抗体,这些结果表明,这些结果表明了与SLEX抗体相互作用的相互作用。通过酪氨酸磷酸化的17 kDa蛋白介导。

项目成果

期刊论文数量(20)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Binding of sialyl Lewis X antigen to lectin-like receptors on NK cells induces cytotoxicity and tyrosine phosphorylation of a 17-kDa protein
Amadori-modified glycated albumin predominantly induces E-selectin expression on human umbilical vein endothelial cells through NADPH oxidase activation
  • DOI:
    10.1016/j.cca.2005.12.008
  • 发表时间:
    2006-05-01
  • 期刊:
  • 影响因子:
    5
  • 作者:
    Higai, K;Shimamura, A;Matsumoto, K
  • 通讯作者:
    Matsumoto, K
Expression of cell surface Lewis X and Y antigens and FUT4 mRNA is increased in Jurkat cells undergoing apoptosis
Amadori-modified glycated human albumin predominantly induces E-selectin expression on human umbilical vein endothelial cells through NADPH oxidase activation
Amadori 修饰的糖化人白蛋白通过 NADPH 氧化酶激活主要诱导人脐静脉内皮细胞上 E-选择素的表达
  • DOI:
  • 发表时间:
    2006
  • 期刊:
  • 影响因子:
    0
  • 作者:
    岡 三喜男;早田 宏;他;S.Abe;Higai Koji
  • 通讯作者:
    Higai Koji
Glycosylation of site-specific glycans of α1-acid glycoprotein and alterations in acute and chronic inflammation
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MATSUMOTO Kojiro其他文献

MATSUMOTO Kojiro的其他文献

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{{ truncateString('MATSUMOTO Kojiro', 18)}}的其他基金

Alteration of site-directed sugar chains of α_1-acid glycoprotein in serum of patients and its clinical significance
患者血清中α_1-酸性糖蛋白定点糖链的改变及其临床意义
  • 批准号:
    13672433
  • 财政年份:
    2001
  • 资助金额:
    $ 2.18万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)

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  • 财政年份:
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