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一种层粘连蛋白样物质在小鼠自然杀伤(NK)淋巴细胞表面的表达及其在NK细胞识别肿瘤靶细胞中的作用。

Expression of a laminin-like substance on the surface of murine natural killer (NK) lymphocytes and its role in NK recognition of tumor target cells.

作者信息

Hiserodt J C, Laybourn K A, Varani J

出版信息

J Immunol. 1985 Aug;135(2):1484-7.

PMID:4008929
Abstract

We have identified a structure on the surface of murine NK cells that is immunochemically cross-reactive with laminin. Treatment of normal CBA/J spleen cells with monospecific anti-laminin serum plus complement completely eliminated NK cytolytic activity against YAC-1 or RL male 1 target cells. In the absence of added complement, spleen cells preincubated with anti-laminin serum were also reduced in their cytolytic activity due to a reduced capacity to bind to the target cells. Treatment with anti-asialo GM1 serum plus complement also eliminated NK activity, but pretreatment of NK cells with anti-asialo GM1 in the absence of complement did not reduce cytolytic activity. Thus, anti-laminin and anti-asialo GM1 bind to structures on the surface of NK cells that distinguish functional (laminin) from nonfunctional (asialo GM1) sites. Flow cytometric analysis revealed that approximately 15% of normal nonadherent splenic lymphocytes expressed laminin-like structures, whereas 16% expressed asialo GM1 and 19% expressed the NK alloantigen NK 2.1. Treatment of alloimmune cytotoxic T lymphocytes (CTL) with anti-laminin plus complement did not affect CTL activity. Thus, anti-laminin serum appears to detect a cell surface structure present on the NK subset of lymphocytes.

摘要

我们在小鼠自然杀伤(NK)细胞表面鉴定出一种结构,该结构与层粘连蛋白存在免疫化学交叉反应。用单特异性抗层粘连蛋白血清加补体处理正常CBA/J脾细胞,可完全消除其对YAC-1或RL雄性1靶细胞的NK细胞溶解活性。在不添加补体的情况下,预先用抗层粘连蛋白血清孵育的脾细胞,由于其与靶细胞结合能力降低,其细胞溶解活性也降低。用抗去唾液酸GM1血清加补体处理也可消除NK活性,但在无补体情况下用抗去唾液酸GM1预处理NK细胞并不会降低细胞溶解活性。因此,抗层粘连蛋白和抗去唾液酸GM1与NK细胞表面的结构结合,这些结构区分了功能性位点(层粘连蛋白)和非功能性位点(去唾液酸GM1)。流式细胞术分析显示,约15%的正常非贴壁脾淋巴细胞表达层粘连蛋白样结构,而16%表达去唾液酸GM1,19%表达NK同种异体抗原NK 2.1。用抗层粘连蛋白加补体处理同种异体免疫细胞毒性T淋巴细胞(CTL)不会影响CTL活性。因此,抗层粘连蛋白血清似乎检测到淋巴细胞NK亚群上存在的一种细胞表面结构。

相似文献

1
Expression of a laminin-like substance on the surface of murine natural killer (NK) lymphocytes and its role in NK recognition of tumor target cells.一种层粘连蛋白样物质在小鼠自然杀伤(NK)淋巴细胞表面的表达及其在NK细胞识别肿瘤靶细胞中的作用。
J Immunol. 1985 Aug;135(2):1484-7.
2
Flow cytometric analysis reveals the presence of asialo GM1 on the surface membrane of alloimmune cytotoxic T lymphocytes.流式细胞术分析显示同种免疫细胞毒性T淋巴细胞表面膜上存在脱唾液酸GM1。
J Immunol. 1986 Mar 1;136(5):1586-91.
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Effect of rabbit anti-asialo GM1 treatment in vivo or with anti-asialo GM1 plus complement in vitro on cytotoxic T cell activities.兔抗去唾液酸GM1体内治疗或抗去唾液酸GM1加补体体外治疗对细胞毒性T细胞活性的影响。
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引用本文的文献

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Cell surface laminin-like substances and laminin-related carbohydrates of rat ascites hepatoma AH7974 and its variants with different lung-colonizing potential.
Clin Exp Metastasis. 1994 May;12(3):203-12. doi: 10.1007/BF01753888.
2
C-reactive protein is involved in natural killer cell-mediated lysis but does not mediate effector-target cell recognition.C反应蛋白参与自然杀伤细胞介导的细胞溶解,但不介导效应细胞与靶细胞的识别。
Immunology. 1987 May;61(1):93-9.
3
Laminin production by murine melanoma cells: possible involvement in cell motility.小鼠黑色素瘤细胞产生层粘连蛋白:可能与细胞运动有关。
Clin Exp Metastasis. 1986 Oct-Dec;4(4):259-72. doi: 10.1007/BF00133591.
4
Inhibition of pluripotent hematopoietic stem cells of bone marrow by large granular lymphocytes.大颗粒淋巴细胞对骨髓多能造血干细胞的抑制作用。
Proc Natl Acad Sci U S A. 1987 Nov;84(21):7691-5. doi: 10.1073/pnas.84.21.7691.
5
Lymphokine-activated killer cells in rats. III. A simple method for the purification of large granular lymphocytes and their rapid expansion and conversion into lymphokine-activated killer cells.大鼠中的淋巴因子激活的杀伤细胞。III. 一种纯化大颗粒淋巴细胞及其快速扩增并转化为淋巴因子激活的杀伤细胞的简单方法。
J Exp Med. 1988 Jan 1;167(1):15-29. doi: 10.1084/jem.167.1.15.
6
Inhibition of human natural killer activity by antiserum against vitamin D-binding protein, a group-specific component (Gc).抗维生素D结合蛋白(一种群体特异性成分,Gc)的抗血清对人类自然杀伤活性的抑制作用。
Clin Exp Immunol. 1989 May;76(2):154-8.
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Biology of natural killer cells.自然杀伤细胞生物学
Adv Immunol. 1989;47:187-376. doi: 10.1016/s0065-2776(08)60664-1.
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