首页> 外文期刊>Cancer Microenvironment >Dendritic Cells (DC) Facilitate Detachment of Squamous Carcinoma Cells (SCC), While SCC Promote an Immature CD16+ DC Phenotype and Control DC Migration
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Dendritic Cells (DC) Facilitate Detachment of Squamous Carcinoma Cells (SCC), While SCC Promote an Immature CD16+ DC Phenotype and Control DC Migration

机译:树突状细胞(DC)促进鳞状细胞癌(SCC)的分离,而SCC促进不成熟的CD16 + DC表型并控制DC迁移。

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In the inflammatory mucosal microenvironment of head and neck SCC (HNSCC), DC express CD16 and are usually in direct contact with tumor cells. Mucosal and inflammation-associated DC develop from monocytes, and monocyte-derived DC are used in HNSCC immunotherapy. However, beyond apoptotic tumor cell uptake and presentation of tumor antigens by DC, HNSCC cell interactions with DC are poorly understood. Using co-cultures of monocyte-derived DC and two established HNSCC cell lines that represent well- and poorly-differentiated SCC, respectively, we found that carcinoma cells induced significant increases in CD16 expression on DC while promoting a CD1a+CD86dim immature phenotype, similar to that observed in HNSCC specimens. Moreover, HNSCC cells affected steady-state and CCL21-induced migration of DC, and these effects were donor-dependent. The CCL21-induced migration directly correlated with HNSCC-mediated effects on CCR7 and CD38 expression on DC-SIGN-high DC. The dominant pattern seen in six out of nine donors was the increase in steady-state and CCL21-induced DC migration in co-cultures with HNSCC, while the reverse pattern, i.e., decreased DC migration in co-cultures with SCC, was identified in two donors. A split in migratory DC behavior, i.e. increase with one HNSCC cell line and a decrease with the second cell line, was observed in one donor. Remarkably, the numbers of live detached HNSCC cells were orders of magnitude higher in DC-HNSCC co-cultures than in parallel HNSCC cell cultures without DC. This study provides novel insights into the effects of DC-HNSCC interactions relevant to the tumor microenvironment.
机译:在头颈SCC(HNSCC)的炎性粘膜微环境中,DC表达CD16,通常与肿瘤细胞直接接触。粘膜和炎症相关的DC由单核细胞形成,单核细胞衍生的DC用于HNSCC免疫治疗。然而,除了凋亡性肿瘤细胞被DC摄取和肿瘤抗原呈递外,对HNSCC细胞与DC的相互作用还知之甚少。使用单核细胞来源的DC和分别代表高分化和低分化SCC的两个已建立的HNSCC细胞系的共培养,我们发现癌细胞诱导DC上CD16表达的显着增加,同时促进CD1a + CD86dim未成熟表型,相似与HNSCC标本中观察到的结果相同。此外,HNSCC细胞影响稳态和CCL21诱导的DC迁移,这些作用是供体依赖性的。 CCL21诱导的迁移与HNSCC介导的对DC-SIGN高DC的CCR7和CD38表达的影响直接相关。在九个供体中,有六个占主导地位的模式是与HNSCC的共培养中稳态和CCL21诱导的DC迁移的增加,而反向模式,即与SCC的共培养中DC迁移的减少,在HNSCC中被发现。两个捐助者。在一个供体中观察到迁移DC行为的分裂,即随着一种HNSCC细胞系增加,而随着第二种细胞系减少。值得注意的是,DC-HNSCC共培养中活离体HNSCC细胞的数量比没有DC的平行HNSCC细胞培养高出几个数量级。这项研究为与肿瘤微环境有关的DC-HNSCC相互作用的影响提供了新颖的见解。

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