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遗传和免疫背景对结直肠腺瘤发展的影响:病例系列报告。

The Influence of the Genetic and Immunologic Context in the Development of Colorectal Adenoma: A Case Series Report.

机构信息

Medical Faculty. University of Porto. Porto. Portugal.

Maastricht University. Maastricht. Netherlands.

出版信息

Acta Med Port. 2020 May 4;33(5):297-304. doi: 10.20344/amp.12462.

Abstract

INTRODUCTION

Overcoming immunosurveillance is a major step in the progression of many types of tumors. Several immune escape strategies have been identified, including immunoediting and the establishment of an immune suppressive microenvironment. The aim of the present study was to determine whether the hereditary or sporadic context has any influence in the relationship between immune surveillance and tumor development, using sporadic and familial adenomatous polyposis related colorectal adenomas as a model.

MATERIAL AND METHODS

The immune tumor-infiltrating cells of a total of 58 low-grade and 18 high-grade colorectal adenomas were examined and compared, using immunostaining for CD3, CD4, CD8, CD57, CD68 and FoxP3.

RESULTS

FoxP3 and CD68 counts were significantly higher in sporadic low-grade dysplasia (p = 0.0003 and p = 0.0103, respectively),and FoxP3 and CD4 counts were found to be significantly higher in high-grade sporadic dysplasia (p = 0.0008 and p = 0.0018, respectively)when compared with corresponding lesions in patients with familial adenomatous polyposis.

DISCUSSION

This study suggests that the immune microenvironment of sporadic and hereditary lesions is different. Sporadic lesions contain a higher number of immune suppressive Treg cells, which suggests a stronger immune selective pressure. In contrast, hereditarylesions seem to benefit from a more tolerant immune microenvironment, allowing for the development of lesions with lower immune cell infiltration.

CONCLUSION

This study shows that sporadic lesions harbor higher tumor-infiltrating immune cell counts, which might reflect a higher immune tolerance towards hereditary lesions.

摘要

简介

克服免疫监视是许多类型肿瘤进展的重要步骤。已经确定了几种免疫逃逸策略,包括免疫编辑和建立免疫抑制微环境。本研究旨在确定遗传性或散发性背景是否对免疫监视与肿瘤发展之间的关系有任何影响,使用散发性和家族性腺瘤性息肉病相关的结直肠腺瘤作为模型。

材料和方法

使用 CD3、CD4、CD8、CD57、CD68 和 FoxP3 的免疫染色,检查并比较了总共 58 例低级别和 18 例高级别结直肠腺瘤的肿瘤浸润免疫细胞。

结果

FoxP3 和 CD68 计数在散发性低级别发育不良中显著更高(p = 0.0003 和 p = 0.0103),FoxP3 和 CD4 计数在高级别散发性发育不良中显著更高(p = 0.0008 和 p = 0.0018)与家族性腺瘤性息肉病患者相应病变相比。

讨论

本研究表明,散发性和遗传性病变的免疫微环境不同。散发性病变含有更多的免疫抑制性 Treg 细胞,这表明更强的免疫选择性压力。相比之下,遗传性病变似乎受益于更耐受的免疫微环境,允许发展免疫细胞浸润较低的病变。

结论

本研究表明,散发性病变具有更高的肿瘤浸润免疫细胞计数,这可能反映了对遗传性病变的更高免疫耐受性。

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