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人肠道中的自然杀伤细胞与自发性细胞介导的细胞毒性

Natural killer cells and spontaneous cell-mediated cytotoxicity in the human intestine.

作者信息

Gibson P R, Dow E L, Selby W S, Strickland R G, Jewell D P

出版信息

Clin Exp Immunol. 1984 May;56(2):438-44.

Abstract

Spontaneous cell-mediated cytotoxicity (SCMC) has been investigated in mononuclear cells (MNC) isolated from intestinal mucosa and autologous peripheral blood from human subjects. The proportion of cells with the NK-K phenotype (Leu 7+) were substantially lower in intestinal MNC than in autologous peripheral blood. SCMC of K-562 target cells when tested at an effector to target (E:T) ratio equivalent to that used for peripheral blood MNC was markedly deficient in intestinal MNC. This was not due to the effect of EDTA and collagenase used in the isolation process. However, at high E:T, ratios, significant cytotoxicity was demonstrated for most intestines examined probably reflecting a low proportion of effector cells within the intestinal MNC population. SCMC in both intestinal and autologous peripheral blood MNC were similarly related to the Leu 7+:T ratios used in the assay indirectly suggesting that the Leu 7+ cell may be responsible for the observed cytotoxicity. It is concluded that the apparent functional difference between similar cells derived from different sites may be largely related to differing proportions of effector cells. The findings indicate the need for specific definition of the effector cell and suggest that intestinal SCMC in health and various disease states requires re-appraisal.

摘要

对从人类受试者的肠黏膜和自体外周血中分离出的单核细胞(MNC)的自发细胞介导细胞毒性(SCMC)进行了研究。具有NK-K表型(Leu 7+)的细胞比例在肠道MNC中显著低于自体外周血。当以与外周血MNC相同的效应细胞与靶细胞比例(E:T)进行测试时,肠道MNC对K-562靶细胞的SCMC明显不足。这并非由于分离过程中使用的EDTA和胶原酶的影响。然而,在高E:T比例下,大多数检测的肠道显示出显著的细胞毒性,这可能反映了肠道MNC群体中效应细胞比例较低。肠道和自体外周血MNC中的SCMC同样与检测中使用的Leu 7+:T比例相关,这间接表明Leu 7+细胞可能是观察到的细胞毒性的原因。得出的结论是,源自不同部位的相似细胞之间明显的功能差异可能在很大程度上与效应细胞的不同比例有关。这些发现表明需要对效应细胞进行具体定义,并提示在健康和各种疾病状态下肠道SCMC需要重新评估。

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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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