• Diogo Garcia, Louisa Spaans, Sara Miranda, Gilza Gonçalves, Joana Reis, José Luís Costa, Cecília Durães, Fátima Carneiro, and José Carlos Machado.
• Medical Faculty. University of Porto. Porto. Portugal.
• Acta Medica Port. 2020 May 4; 33 (5): 297-304.

IntroductionOvercoming 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 MethodsThe 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.ResultsFoxP3 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.DiscussionThis 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.ConclusionThis study shows that sporadic lesions harbor higher tumor-infiltrating immune cell counts, which might reflect a higher immune tolerance towards hereditary lesions.

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