Induction of tumor-specific T cell memory by NK cell-mediated tumor rejection
Induction of tumor-specific T cell memory by NK cell-mediated tumor rejection
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DOI：
10.1038/ni746
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发表时间：
2002-01-01
影响因子：
30.5
通讯作者：
Smyth, MJ
中科院分区：
文献类型：
--
作者：
Kelly, JM;Darcy, PK;Smyth, MJ
自然杀伤（NK）细胞可以调节适应性免疫反应的发展，但到目前为止，几乎没有证据支持这一假设。我们研究了表达CD 70并与NK细胞上组成型表达的CD 70配体（CD 27）相互作用的各种肿瘤细胞系引起的原发性和继发性免疫。CD 70表达增强了体内原发性肿瘤排斥以及针对继发性肿瘤攻击的T细胞免疫。主要组织相容性复合物（MHC）I类缺陷RMA-S的原发性排斥反应。CD 70肿瘤细胞介导的NK细胞和穿孔素和干扰素-γ依赖的机制。这种NK细胞介导的过程也有效地诱发了随后对亲本、MHC I类足够的RMA肿瘤细胞的肿瘤特异性细胞毒性和T辅助细胞I型应答的发展。因此，CD 27-CD 70相互作用提供了先天性NK细胞应答和适应性T细胞免疫之间的关键联系。
Natural killer (NK) cells may modulate the development of adaptive immune responses, but until now there has been little evidence to support this hypothesis. We investigated the primary and secondary immunity elicited by various tumor cell lines that express CD70 and interact with CD70 ligand (CD27), which is constitutively expressed on NK cells. CD70 expression enhanced primary tumor rejection in vivo as well as T cell immunity against secondary tumor challenge. Primary rejection of major histocompatibility complex (MHC) class I-deficient RMA-S.CD70 tumor cells was mediated by NK cells and perforin- and interferon-gamma-dependent mechanisms. This NK cell-mediated process also efficiently evoked the subsequent development of tumor-specific cytotoxic and T helper type I responses to the parental, MHC class I-sufficient, RMA tumor cells. Thus CD27-CD70 interactions provide a key link between innate NK cell responses and adaptive T cell immunity.