Analyses of anti-tumor immune responses in the sentinel lymph nodes from the patients with oral

B7-H1是免疫调节分子PD-1的配体之一。我们对小鼠口腔鳞状细胞癌细胞系NRS1的研究发现，内源性诱导的B7-H1通过PD-1负性调节NRS1细胞的抗肿瘤免疫反应。相比之下，B7-H1。通过基因转导高水平表达，以pd -1不依赖的方式增强抗肿瘤反应。这些结果表明，b7 - h1介导的免疫调节似乎是非常复杂的。一方面，B7-H1也被PD-1的另一个配体B7-DC诱导到树突状细胞（DC）上。与B7-H1不同，B7-DC可选择性诱导DC。在半抗原致敏后的引流淋巴结中，CD86^<高> DC与从皮肤迁移的CD11b^+CD11c^+ DC共表达B7-DC。半成熟DC表达低水平CD86，表达B7-H1，不表达B7-DC。在半抗原致敏时给予抗b7 - h1或抗pd -1单克隆抗体增强了半抗原的应答。这些结果表明PD-1:B7-H1通路参与了耐受性诱导。将高度转移的NRS1细胞接种到舌中，可诱导引流LN中CD11b^<++>大细胞快速扩增。这些细胞表达低CD86和B7-H1，似乎诱导前哨淋巴结耐受。我们的研究结果表明，前哨LN中迁移的DC可能引起了耐受性诱导，这取决于B7-H1。

B7-H1 is one of ligands for an immunoregulatory molecule, PD-1. Our studies using a murine oral squamous cell carcinoma cell line, NRS1 revealed that the endogenously induced B7-H1 on NRS1 cells regulated negatively anti-tumor immune responses through PD-1. In contrast, the B7-H1. expressed at H1gh levels by gene transduction enhanced the antitumor responses in a PD-1-independent manner. These results suggest that B7-H1-mediated immune regulation seems to be very complicated.On one hand, B7-H1 is also induced on dendritic cells (DC) with B7-DC, wH1ch is another ligand for PD-1. Unlike B7-H1, B7-DC is selectively induced on DC. In the draining lymph nodes after the hapten sensitization, CD86^<high> DC co-expressed B7-DC witH1n the migrating CD11b^+CD11c^+ DC from the skin. The semi-mature DC, wH1ch expressed low levels of CD86 expressed B7-H1 but not B7-DC. The administration of anti-B7-H1 or anti-PD-1 monoclonal antibody at the hapten-sensitization enhanced the responses to the hapten-challenge. These results suggest that the PD-1:B7-H1 pathway is involved in tolerance induction.The inoculation of H1ghly metastatic NRS1 cells into the tongue induced a rapid expansion of CD11b^<++> large cells in the draining LN. These cells expressed low CD86 and B7-H1 and seem to induce tolerance in the sentinel LN. Our results suggest the possibility that the migrated DC in the sentinel LN caused tolerance induction, wH1ch is dependent upon B7-H1.