丛状神经纤维瘤 (PNF) 是一种良性神经肿瘤，由雪旺细胞中 NF1 肿瘤抑制因子的缺失引起。 PNFs富含免疫细胞，但免疫细胞是否是肿瘤发生所必需的尚不清楚。我们发现，抑制干扰素基因刺激物 (STING) 可减少血浆 CXCL10、肿瘤 T 细胞和树突状细胞 (DC) 的募集以及肿瘤形成。此外，缺乏 XCR-1 DC 的小鼠表现出肿瘤浸润 T 细胞和 PNF 肿瘤减少。来自荷瘤小鼠的抗原呈递细胞在体外促进 CD8 T 细胞增殖，PNF T 细胞表达高水平的 CCL5，表明 T 细胞激活。值得注意的是，Rag1-/- 中不存在肿瘤和神经相关巨噬细胞； Nf1f/f； DhhCre 小鼠和来自荷瘤小鼠的 CD8 T 细胞的过继转移恢复了 PNF 的启动。在这种情况下，PNF 在随后的 T 细胞去除后缩小。因此，STING 通路激活有助于 PNF 启动和维持所需的 CD8 T 细胞依赖性炎症反应。

Plexiform neurofibromas (PNFs) are benign nerve tumors driven by loss of the NF1 tumor suppressor in Schwann cells. PNFs are rich in immune cells, but whether immune cells are necessary for tumorigenesis is unknown. We show that inhibition of stimulator of interferon gene (STING) reduces plasma CXCL10, tumor T cell and dendritic cell (DC) recruitment, and tumor formation. Further, mice lacking XCR-1+ DCs showed reduced tumor-infiltrating T cells and PNF tumors. Antigen-presenting cells from tumor-bearing mice promoted CD8+ T cell proliferation in vitro, and PNF T cells expressed high levels of CCL5, implicating T cell activation. Notably, tumors and nerve-associated macrophages were absent in Rag1-/-; Nf1f/f; DhhCre mice and adoptive transfer of CD8+ T cells from tumor-bearing mice restored PNF initiation. In this setting, PNF shrunk upon subsequent T cell removal. Thus, STING pathway activation contributes to CD8+ T cell-dependent inflammatory responses required for PNF initiation and maintenance.