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首页> 外文期刊>Immunology: An Official Journal of the British Society for Immunology >Dissection of spontaneous cytotoxicity by human intestinal intraepithelial lymphocytes: MIC on colon cancer triggers NKG2D-mediated lysis through Fas ligand.
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Dissection of spontaneous cytotoxicity by human intestinal intraepithelial lymphocytes: MIC on colon cancer triggers NKG2D-mediated lysis through Fas ligand.

机译：人肠上皮内淋巴细胞对自发细胞毒性的解剖：结肠癌上的MIC通过Fas配体触发NKG2D介导的裂解。

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Human intestinal intraepithelial lymphocytes (IELs), which are T-cell receptor alphabeta+ CD8+ T cells located between epithelial cells (ECs), are likely to participate in the innate immune response against colon cancer. IELs demonstrate spontaneous cytotoxic (SC) activity specifically directed against EC tumours but not against other solid tumour types. The aim of this study was to dissect out the mechanism of SC activity, focusing on the interaction of NKG2D on IELs with its ligands [major histocompatibility complex (MHC) class I chain-related protein (MIC) and UL16 binding protein (ULBP)] found mainly on EC tumours. A novel series of events occurred. The NKG2D-MIC/ULBP interaction induced Fas ligand (FasL) production and FasL-mediated SC activity against HT-29 cells and MIC-transfectants. Tumour necrosis factor-alpha and interferon-gamma, produced independently of this interaction, promoted SC activity. The immune synapse was strengthened by the interaction of CD103 on IELs with E-cadherin on HT-29 cells. Neither T-cell receptor nor MHC class I was involved. While the HT-29 cells were destroyed by soluble FasL, tumour necrosis factor-alpha and interferon-gamma, the IELs were resistant to the effects of these mediators and to FasL expressed by the HT-29 cells. This unidirectional FasL-mediated cytotoxicity of IELs against HT-29 cells, triggered through NKG2D, is unique and is likely to be a property of those CD8+ tumour-infiltrating lymphocytes that phenotypically resemble IELs.
机译：人肠上皮内淋巴细胞（IEL）是位于上皮细胞（EC）之间的T细胞受体字母+ CD8 + T细胞，可能参与针对结肠癌的先天免疫应答。 IELs表现出针对EC肿瘤的自发细胞毒（SC）活性，但不针对其他实体瘤类型。这项研究的目的是剖析SC活性的机制，着重于NEL在IELs上与其配体的相互作用[主要组织相容性复合物（MHC）I类链相关蛋白（MIC）和UL16结合蛋白（ULBP）]。主要见于EC肿瘤。发生了一系列新颖的事件。 NKG2D-MIC / ULBP相互作用诱导Fas配体（FasL）的产生和FasL介导的针对HT-29细胞和MIC-转染子的SC活性。独立于这种相互作用而产生的肿瘤坏死因子-α和干扰素-γ促进了SC活性。 IELs上的CD103与HT-29细胞上的E-钙黏着蛋白的相互作用增强了免疫突触。 T细胞受体和MHC I类均未涉及。尽管HT-29细胞被可溶性FasL，肿瘤坏死因子-α和干扰素-γ破坏，但IEL对这些介体的作用和HT-29细胞表达的FasL均具有抗性。通过NKG2D触发的这种FasL介导的IEL对HT-29细胞的单向细胞毒性是独特的，并且可能是那些表型类似于IEL的CD8 +肿瘤浸润淋巴细胞的特性。

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