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通过NK1.1发出的信号会触发自然杀伤细胞死亡,但会诱导自然杀伤T细胞产生白细胞介素-4。

Signalling through NK1.1 triggers NK cells to die but induces NK T cells to produce interleukin-4.

作者信息

Asea A, Stein-Streilein J

机构信息

Department of Medicine, University of Miami School of Medicine, FL, USA.

出版信息

Immunology. 1998 Feb;93(2):296-305. doi: 10.1046/j.1365-2567.1998.00422.x.

DOI:10.1046/j.1365-2567.1998.00422.x
PMID:9616382
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1364192/
Abstract

In vivo inoculation of specific antibody is an accepted protocol for elimination of specific cell populations. Except for anti-CD3 and anti-CD4, it is not known if the depleted cells are eliminated by signalling through the target molecule or through a more non-specific mechanism. C57BL/6 mice were inoculated with anti-natural killer (NK1.1) monoclonal antibody (mAb). Thereafter spleen cells were harvested, stained for both surface and intracellular markers, and analysed by flow cytometry. As early as 2 hr post inoculation, NK cells were signalled to become apoptotic while signalling through the NK1.1 molecule activated NK1.1+ T-cell receptor (TCR)+ (NK T) cells to increase in number, and produce interleukin-4 (IL-4). Anti NK1.1 mAb was less efficient at signalling apoptosis in NK cells when NK T-cell deficient [beta 2-microglobulin beta 2m-deficient] mice were used compared with wild type mice. Efficient apoptotic signalling was restored when beta 2m-deficient mice were reconstituted with NK T cells. NK-specific antibody best signals the apoptotic process in susceptible NK cells when resistant NK T cells are present, activated, and secrete IL-4.

摘要

体内接种特异性抗体是清除特定细胞群体的一种公认方案。除抗CD3和抗CD4外,尚不清楚被清除的细胞是通过靶分子信号传导还是通过更非特异性的机制被清除。给C57BL/6小鼠接种抗自然杀伤细胞(NK1.1)单克隆抗体(mAb)。此后收集脾细胞,对表面和细胞内标志物进行染色,并通过流式细胞术进行分析。接种后早在2小时,NK细胞就被信号传导诱导凋亡,而通过NK1.1分子的信号传导激活了NK1.1 + T细胞受体(TCR)+(NK T)细胞,使其数量增加并产生白细胞介素-4(IL-4)。与野生型小鼠相比,当使用NK T细胞缺陷型(β2-微球蛋白β2m缺陷型)小鼠时,抗NK1.1 mAb在诱导NK细胞凋亡信号传导方面效率较低。当用NK T细胞重建β2m缺陷型小鼠时,有效的凋亡信号传导得以恢复。当抗性NK T细胞存在、被激活并分泌IL-4时,NK特异性抗体在易感NK细胞中对凋亡过程发出的信号最佳。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c092/1364192/eb001b2a7c56/immunology00046-0165-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c092/1364192/eb001b2a7c56/immunology00046-0165-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c092/1364192/eb001b2a7c56/immunology00046-0165-a.jpg

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