Tumor-draining lymph nodes (TDLNs) are critical organs, where activation of B cells and T cells is orchestrated. Effector or regulatory anti-tumor immune responses are reflected by the composition of the lymphocytic and monocytic cell population of the node. Aside from the migratory cancer cell abilities, immune cell phenotypic changes in the TDLNs may define nodal invasion by cancer. We assessed the qualitative and quantitative differences between lymphocytic phenotypes in regional TDLNs, in 20 node-negative and 20 node-positive patients (involved and uninvolved nodes) with rectal adenocarcinomas. Benign reactive nodes were also analyzed. CD8+ cells, the main source of cytotoxic T cells, were increased in all TDLNs and, even stronger, in the involved nodes. The percentage of CD4+ cells were significantly increased in negative and uninvolved nodes, while the CD4/CD8 ratio was significantly lower in involved TDLNs. CD25+ and FOXP3+ regulatory lymphocytes, however, prevailed in involved nodes, while uninvolved and negative nodes had a low presence of these regulatory cells. CD20+ B cells were also more abundant in involved nodes. PD-1+ lymphocytes were localized in the germinal centers. A significantly lower percentage of PD-1+ lymphocytes were noted in involved nodes. The development of a regulatory lymphocytic phenotype in the TDLNs appears as an important mechanism that allows cancer cell installation into the nodal environment. As negative/uninvolved TDLNs had a less severe immunosuppression, it is postulated that secreted molecules by cancer cells gradually attenuate the anti-tumor defenses of the TDLNs allowing the subsequent intra-nodal growth of cancer.

肿瘤引流淋巴结 (TDLN) 是关键器官，在那里协调 B 细胞和 T 细胞的激活。效应或调节性抗肿瘤免疫反应由淋巴结的淋巴细胞和单核细胞群的组成反映。除了癌细胞的迁移能力外，TDLN 中的免疫细胞表型变化可能定义了癌症的淋巴结侵袭。我们评估了 20 名淋巴结阴性和 20 名淋巴结阳性患者（受累和未受累淋巴结）的直肠腺癌区域性 TDLN 淋巴细胞表型之间的定性和定量差异。还分析了良性反应节点。CD8+ 细胞是细胞毒性 T 细胞的主要来源，在所有 TDLN 中都增加，并且在所涉及的节点中甚至更强。CD4+ 细胞的百分比在阴性和未受累的淋巴结中显着增加，而在受累的 TDLN 中 CD4/CD8 比率显着降低。CD25+ 和 FOXP3+ 调节性淋巴细胞，然而，在涉及的节点中占主导地位，而未涉及的和消极的节点则这些调节细胞的存在率很低。CD20+ B 细胞在受累淋巴结中也更丰富。PD-1+ 淋巴细胞位于生发中心。在受累淋巴结中注意到 PD-1+ 淋巴细胞的百分比显着降低。TDLN 中调节淋巴细胞表型的发展似乎是一种重要机制，允许癌细胞安装到淋巴结环境中。由于阴性/未受累的 TDLN 具有较轻的免疫抑制，因此推测癌细胞分泌的分子会逐渐减弱 TDLN 的抗肿瘤防御，从而允许随后的癌症在淋巴结内生长。CD20+ B 细胞在受累淋巴结中也更丰富。PD-1+ 淋巴细胞位于生发中心。在受累淋巴结中注意到 PD-1+ 淋巴细胞的百分比显着降低。TDLN 中调节淋巴细胞表型的发展似乎是一种重要机制，允许癌细胞安装到淋巴结环境中。由于阴性/未受累的 TDLN 具有较轻的免疫抑制，因此推测癌细胞分泌的分子会逐渐减弱 TDLN 的抗肿瘤防御，从而允许随后的癌症在淋巴结内生长。CD20+ B 细胞在受累淋巴结中也更丰富。PD-1+ 淋巴细胞位于生发中心。在受累淋巴结中注意到 PD-1+ 淋巴细胞的百分比显着降低。TDLN 中调节淋巴细胞表型的发展似乎是一种重要机制，允许癌细胞安装到淋巴结环境中。由于阴性/未受累的 TDLN 具有较轻的免疫抑制，因此推测癌细胞分泌的分子会逐渐减弱 TDLN 的抗肿瘤防御，从而允许随后的癌症在淋巴结内生长。TDLN 中调节淋巴细胞表型的发展似乎是一种重要机制，允许癌细胞安装到淋巴结环境中。由于阴性/未受累的 TDLN 具有较轻的免疫抑制，因此推测癌细胞分泌的分子会逐渐减弱 TDLN 的抗肿瘤防御，从而允许随后的癌症在淋巴结内生长。TDLN 中调节淋巴细胞表型的发展似乎是一种重要机制，允许癌细胞安装到淋巴结环境中。由于阴性/未受累的 TDLN 具有较轻的免疫抑制，因此推测癌细胞分泌的分子会逐渐减弱 TDLN 的抗肿瘤防御，从而允许随后的癌症在淋巴结内生长。