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同基因B淋巴瘤细胞对基因背景下自然杀伤(NK)细胞数量低的SJL/J小鼠的NK细胞提供了独特的刺激。

Syngeneic B lymphoma cells provide a unique stimulus to natural killer (NK) cells in genetically low-NK SJL/J mice.

作者信息

Lin T Z, Ponzio N M

机构信息

Department of Laboratory Medicine and Pathology, UMDNJ-New Jersey Medical School, Newark 07103.

出版信息

J Leukoc Biol. 1991 Jan;49(1):48-57. doi: 10.1002/jlb.49.1.48.

Abstract

SJL/J mice are a genetically low-NK strain, and their cytotoxic activity cannot be augmented with conventional NK inducers. In contrast, effector cells taken from the lymphoid tissues of SJL mice bearing a syngeneic B cell lymphoma (RCS) show variable, but significant levels of cytotoxic activity against NK-susceptible targets, such as YAC-1. Previous results suggested that the RCS cells themselves contributed to this cytotoxicity. However, results presented here indicate the most, if not all of the activity present within the lymphoid tissues of RCS-bearing mice is mediated by RCS-activated, host NK cells. These results were confirmed by in vitro studies, which demonstrate that both gamma irradiated (gamma-) RCS cells and gamma-allogeneic spleen cells induce cytotoxic activity in SJL spleen cells against YAC targets. However, the cytotoxicity induced by gamma-allogeneic cells is mediated largely by lymphokine-activated killer (LAK) cells, since these effectors also lyse NK-resistant target cells, such as L1210. In contrast, the cytotoxic effector cells that are induced by syngeneic gamma-RCS cells cause lysis of YAC targets, but not L1210 target cells. These data indicate that the syngeneic B cell lymphomas of SJL mice are a unique stimulus for host NK cells in this strain. Since activated NK cells produce a variety of lymphokines, RCS stimulation of host NK cells in SJL mice may provide some of the growth-promoting lymphokines that are known to be necessary for progressive growth of these lymphoma cells.

摘要

SJL/J小鼠是一种基因上NK细胞数量低的品系,其细胞毒性活性不能通过传统的NK细胞诱导剂增强。相比之下,从携带同基因B细胞淋巴瘤(RCS)的SJL小鼠的淋巴组织中获取的效应细胞对NK敏感靶标(如YAC-1)表现出可变但显著的细胞毒性活性水平。先前的结果表明RCS细胞本身促成了这种细胞毒性。然而,此处呈现的结果表明,携带RCS的小鼠淋巴组织中存在的大部分(如果不是全部)活性是由RCS激活的宿主NK细胞介导的。这些结果通过体外研究得到证实,该研究表明γ射线照射的(γ-)RCS细胞和γ异基因脾细胞均可诱导SJL脾细胞对YAC靶标的细胞毒性活性。然而,γ异基因细胞诱导的细胞毒性很大程度上是由淋巴因子激活的杀伤细胞(LAK)介导的,因为这些效应细胞也能裂解NK抗性靶标细胞,如L1210。相比之下,同基因γ-RCS细胞诱导的细胞毒性效应细胞可导致YAC靶标细胞裂解,但不能导致L1210靶标细胞裂解。这些数据表明,SJL小鼠的同基因B细胞淋巴瘤对该品系中的宿主NK细胞是一种独特的刺激。由于活化的NK细胞产生多种淋巴因子,SJL小鼠中RCS对宿主NK细胞的刺激可能提供了一些已知对这些淋巴瘤细胞的渐进性生长所必需的促生长淋巴因子。

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