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肽聚糖单体(PGM)对小鼠脾细胞NK及ADCC活性的体内和体外调节

In vivo and in vitro modulation of NK and ADCC activities of mouse spleen cells by peptidoglycan monomer (PGM).

作者信息

Gabrilovac J, Tomasić J, Boranić M, Martin-Kleiner I, Osmak M

机构信息

Dep. of Experimental Biology and Medicine, Ruder Bosković Institute, Zagreb, Yugoslavia.

出版信息

Res Exp Med (Berl). 1989;189(4):265-73. doi: 10.1007/BF01852258.

Abstract

The ability of peptidoglycan monomer (PGM), an immunomodulator obtained from Brevibacterium divaricatum, to modulate NK and ADCC activities of spleen cells was tested in mice with constitutively weak (C57B1) or strong NK activity (CBA, C3H). In weak reactors, i.v. injection of PGM enhanced the NK and ADCC activity as effectively as a known stimulator, poly I.C, and the dynamics of the response was comparable. In strong reactors, PGM caused two peaks of the ADCC response, and one peak of NK stimulation (after an initial decline), whereas poly I.C caused more or less persistent stimulation of both activities. Incubation of spleen cells with PGM was generally less effective than the treatment in vivo. No alteration of NK activity was recorded at high effector-to-target ratio (E:T), and at low ones, PGM caused suppression. This was true both for weakly and strongly reactive cells. ADCC was either unchanged (CBA spleen cells), stimulated (C3H), or suppressed at high E:T and enhanced at low E:T (C57B1). PGM apparently activates an interlocked regulatory mechanism, and the final outcome probably depends on relative concentrations of regulatory and effector cells and on their per cell activities. Hence the effect varied with the time interval between treatment and assay, with strain-related constitutive reactivity, and with the E:T ratio.

摘要

对从分叉短杆菌中获得的免疫调节剂肽聚糖单体(PGM)调节脾脏细胞NK和ADCC活性的能力,在具有组成性弱NK活性(C57B1)或强NK活性(CBA、C3H)的小鼠中进行了测试。在弱反应小鼠中,静脉注射PGM增强NK和ADCC活性的效果与已知刺激剂聚肌胞苷酸(poly I.C)一样有效,且反应动力学相当。在强反应小鼠中,PGM引起ADCC反应的两个峰值和NK刺激的一个峰值(在最初下降之后),而聚肌胞苷酸对两种活性或多或少有持续刺激作用。用PGM孵育脾脏细胞通常比体内治疗效果差。在高效应物与靶细胞比例(E:T)下未记录到NK活性的改变,而在低比例下,PGM会导致抑制。弱反应和强反应细胞均如此。ADCC在高E:T时要么未改变(CBA脾脏细胞)、受到刺激(C3H),要么受到抑制,而在低E:T时增强(C57B1)。PGM显然激活了一种连锁调节机制,最终结果可能取决于调节细胞和效应细胞的相对浓度及其每细胞活性。因此,效应随治疗与检测之间的时间间隔、与品系相关的组成性反应性以及E:T比例而变化。

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