Activated, but not resting, T cells can be recognized and killed by syngeneic NK cells
Activated, but not resting, T cells can be recognized and killed by syngeneic NK cells
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DOI：
10.4049/jimmunol.170.7.3572
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发表时间：
2003-04-01
影响因子：
4.4
通讯作者：
Miller, RG
中科院分区：
文献类型：
--
作者：
Rabinovich, BA;Li, J;Miller, RG
我们证明了IL-2激活的NK细胞或淋巴因子激活的杀伤细胞识别并杀死已被APC激活的同源CD 4（+）和CD 8（+）T细胞。APC的诱导需要TCR特异性Ag，并且裂解是穿孔素介导的。布雷菲德菌素A，破坏蛋白质转运，抑制敏感性，诱导激活。在BALB/c中，NKG 2D配体的表达与溶解相关，并可被布雷菲德菌素A抑制。同样，在杀伤试验中加入抗NKG 2D mAb可完全消除裂解。将小鼠NKG 2D转导至人NK细胞系YTSeco中，赋予其杀死活化的BALB/c T细胞的能力，表明NKG 2D是识别所必需的。我们的数据为研究NK细胞在T细胞调节中的作用提供了基础。
We demonstrate that IL-2-activated NK cells or lymphokine-activated killer cells recognize and kill syngeneic CD4(+) and CD8(+) T cells that have been activated by APCs. Induction with APC required TCR-specific Ag, and lysis was perforin mediated. Brefeldin A, which disrupts protein transport, inhibited the sensitivity, induced by activation. In BALB/c, expression of NKG2D ligands correlated with lysis and could be inhibited by brefeldin A. As well, addition of anti-NKG2D mAb to a killing assay completely abrogated lysis. Transduction of mouse NKG2D into a human NK cell line, YTSeco, conferred upon it the ability to kill activated BALB/c T cells, indicating that NKG2D is necessary for recognition. Our data provide a basis for studying a role for NK cells in T cell regulation.