80%的梅尔克细胞癌（MCC）病例的发病机制与梅尔克细胞多瘤病毒（MCPyV）相关。我们评估了叉头螺旋转录因子P3（FOXP3）和具有免疫球蛋白和免疫受体酪氨酸基反应性抑制基序（TIGIT）-CD155途径，这些是免疫治疗的靶点，作为MCC的预后因素。我们分析了111例MCC患者的mRNA表达数据，并进行免疫组化分析，以检测65个MCC病例中程序性死亡配体1（PD-L1）、CD8、FOXP3、TIGIT和CD155的表达。在CD8和FOXP3免疫染色中，我们通过将区域分为肿瘤中心和浸润前缘区域，确定了表达浸润细胞的数量。FOXP3的表达分别在具有高和低强度的细胞中进行评估。我们观察到MCC细胞中存在异常的TIGIT表达和弱的CD155染色。CD8和FOXP3阳性细胞浸润在浸润前缘区比肿瘤中心更高。多变量Cox危害分析显示，浸润前缘中强度低的FOXP3表达密度高是一种有利的预后因素（p=0.025）。因此，针对TIGIT-CD155信号通路以及FOXP3和PD-L1可能是MCC的治疗策略。© 2023. Springer Nature Limited.

The pathogenesis of 80% of Merkel cell carcinoma (MCC) cases is associated with Merkel cell polyomavirus (MCPyV). Forkhead helix transcription factor P3 (FOXP3) and the T cell immunoreceptor with immunoglobulin and immunoreceptor tyrosine-based inhibition motif domains (TIGIT)-CD155 pathway, which are targets for immunotherapy, were assessed as prognostic factors of MCC. We analyzed mRNA expression data of 111 patients with MCC and performed immunohistochemical analysis to detect the expression of programmed death ligand 1 (PD-L1), CD8, FOXP3, TIGIT, and CD155 in 65 cases of MCC. In CD8 and FOXP3 immunostaining, the number of expressing-infiltrating cells was determined by dividing the region into tumor center and invasive front areas. FOXP3 expression was evaluated separately in cells with high and low intensities. Aberrant TIGIT expression and weak CD155 staining were observed in MCC cells. CD8- and FOXP3-positive cell infiltrations were higher in the invasive front than in the tumor center. Multivariate Cox hazard analysis revealed that high infiltration of cells with low-intensity FOXP3 expression in the invasive front is a favorable prognostic factor (p = 0.025). Thus, targeting TIGIT-CD155 signaling and FOXP3 as well as PD-L1 may be a therapeutic strategy for MCC.© 2023. Springer Nature Limited.