NKG2D公司
MHC I级
细胞毒性T细胞
主要组织相容性复合体
自然杀伤细胞
细胞
淋巴因子激活杀伤细胞
分子生物学
细胞培养
生物
细胞生物学
化学
细胞毒性
免疫系统
白细胞介素12
癌症研究
免疫学
体外
生物化学
遗传学
作者
Antonio E. Serrano,Evelyn Menares-Castillo,Macarena Garrido‐Tapia,Carolina Ribeiro,Carolina Hernández,Ariadna Mendoza-Naranjo,Marcela Gatica-Andrades,Rodrigo Valenzuela-Díaz,Roberto Ariel Abeldaño Zúñiga,Mercedes López,Flavio Salazar‐Onfray,Juan-Carlos Aguillón,María-Carmen Molina
摘要
Natural-killer group 2, member D (NKG2D) binds to a variety of ligands, including the major histocompatibility complex (MHC) class I chain-related proteins (MIC) and UL16-binding proteins (ULBP). It is regarded as a co-activating receptor on NK cells, having an important role in the cell-mediated immune response to tumours. We studied the influence of interleukin (IL)-10 on the regulation of MIC and ULBP expression on melanoma cells, and its effect on the cytotoxic function of NK cells in vitro. Here, we show that, in the presence of IL-10, FMS mel and BL mel cell lines decreased MICA and ULBP2 surface expression, whereas MHC class I did not change substantially on the cell surface. MICA mRNA levels decreased in IL-10-treated FMS and IL-10-transduced BL cell lines. Interestingly, we observed that MICB surface expression and its mRNA levels increased upon IL-10 treatment in a melanoma cell line. These changes in NKG2D ligands surface expression patterns owing to IL-10 treatment resulted in an effect on lysis susceptibility mediated by lymphocyte-activated killer cells, as tumour cell lines that displayed a higher decrease of MICA on their surface had lower levels of lysis. In addition, expression of CD107a was downregulated on the surface of NK cells following stimulation with IL-10-treated FMS cells. Our results suggest a novel function for IL-10 in the modulation of NKG2D ligand expression and in the control of cytotoxicity mediated by NKG2D/NKG2D ligand axis.
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