TGF-β downregulates the activating receptor NKG2D on NK cells and CD8+ T cells glioma patients
TGF-β downregulates the activating receptor NKG2D on NK cells and CD8+ T cells glioma patients
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DOI：
10.1093/neuonc/nop009
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发表时间：
2010-01-01
期刊：
影响因子：
15.9
通讯作者：
Parsa, Andrew T.
中科院分区：
文献类型：
--
作者：
Crane, Courtney A.;Han, Seunggu J.;Parsa, Andrew T.
激活受体NKG2D由自然杀伤细胞（NK）和CD8(+) T细胞表达，具有特异性杀伤转化细胞的作用。我们检测了NKG2D在多形性胶质母细胞瘤患者中的表达，发现NKG2D在NK细胞和CD8(+) T细胞上下调。肿瘤切除后，淋巴细胞上NKG2D的表达显著增加，并与NKG2D配体阳性肿瘤靶点杀伤能力的增强相关。尽管胶质母细胞瘤患者血清中存在可溶性NKG2D配体，但NKG2D下调主要是由肿瘤源性肿瘤生长因子- β引起的，这表明阻断该细胞因子可能具有治疗益处。
The activating receptor NKG2D, expressed by natural killer (NK) cells and CD8(+) T cells, has a role in the specific killing of transformed cells. We examined NKG2D expression In patients with glioblastoma multiforme and found that NKG2D was downregulated on NK cells and CD8(+) T cells. Expression of NKG2D on lymphocytes significantly increased following tumor resection and correlated with all increased ability to kill NKG2D ligand-positive tumor targets. Despite the presence of soluble NKG2D ligands in the sera of glioblastoma patients, NKG2D downregulation was primarily caused by tumor-derived tumor growth factor-beta, suggesting that blocking of this cytokine may have therapeutic benefit.