Esophageal adenocarcinoma (EAC) is the final step of a pathway starting with esophageal reflux disease, Barrett's metaplasia and Barrett's dysplasia. Positive costimulatory ligands such as CD80 have been suggested to contribute to anti-tumor T-cell efficacy. Here we report for the first time the role of CD80 in the inflammatory esophageal carcinogenesis and characterize the immune environment of EAC. Mucosa samples from cancer were obtained during esophagectomy from patients affected by EAC. Fresh biopsies were obtained from patients who underwent endoscopy for screening or follow-up. A rodent model of reflux induced esophageal carcinogenesis was created with an esophago-gastro-jejunostomy. CD80 expression was increased in epithelial cells during metaplasia in the inflammatory esophageal carcinogenesis cascade. Cd80 null mice as well as WT mice that received antiCD80 antibodies showed a higher rate of dysplasia and KI-67+ cells. These results suggest that CD80 mediates an active immune surveillance process in early inflammation-driven esophageal carcinogenesis.

中文翻译：

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CD80表达促进巴雷特化生组织中的免疫监视。

食道腺癌（EAC）是从食道反流病，巴雷特化生和巴雷特不典型增生开始的途径的最后一步。已建议使用阳性共刺激配体（例如CD80）来增强抗肿瘤T细胞的功效。在这里，我们首次报告CD80在食管炎性癌变中的作用，并表征了EAC的免疫环境。在食管切除术中从受EAC影响的患者中获得了癌症的粘膜样本。从接受内窥镜检查或随访的患者获得新鲜的活组织检查。用食管-胃-空肠造口术建立了反流诱导的食管癌变的啮齿动物模型。在炎性食管癌变过程中，化生过程中上皮细胞CD80表达增加。接受抗CD80抗体的Cd80无效小鼠和WT小鼠显示出异型增生和KI-67 +细胞的发生率更高。这些结果表明，CD80在早期炎症驱动的食管癌变过程中介导了主动的免疫监视过程。