CD8 T cells can kill malignant cells in an antigen-specific manner. However, anti-tumoral responses are usually limited by suppressive factors that curb the effector responses of tumor-infiltrating CD8 T cells. Therapeutic strategies to overcome intra-tumoral T cell suppression, for example immune checkpoint inhibition, have been clinically effective in patients with cancer. Here, we provide data that demonstrates that GK-1, a peptide derived from the parasite Taenia crassiceps, promotes an anti-melanoma CD8 T cell response with heightened effector characteristics that leads to an increased amount of tumor-infiltrating CD44⁺ IFN-γ-producing CD8 T cells. The response induced by GK-1 was associated with a reduction in the expression of PD-1 and PD-L1 on tumor-infiltrating CD8 and dendritic cells, respectively, effects that led to a dramatic decrease in tumor burden. Our results suggest that the immunomodulatory properties of GK-1 may promote a CD8 T cell response that may be therapeutically useful in the setting of cancer.

CD8 T细胞可以以抗原特异性方式杀死恶性细胞。但是，抗肿瘤反应通常受到抑制肿瘤浸润CD8 T细胞效应反应的抑制因子的限制。克服肿瘤内T细胞抑制（例如免疫检查点抑制）的治疗策略在癌症患者中已经在临床上有效。在这里，我们提供的数据证明，GK-1（一种来自寄生虫Ta虫（Taenia crassiceps）的肽）可促进抗黑素瘤CD8 T细胞反应，并具有增强的效应子特性，从而导致肿瘤浸润CD44 ^+的数量增加产生IFN-γ的CD8 T细胞。GK-1诱导的反应分别与肿瘤浸润性CD8和树突状细胞上PD-1和PD-L1的表达降低有关，这种作用导致肿瘤负荷显着降低。我们的结果表明，GK-1的免疫调节特性可能会促进CD8 T细胞应答，这可能在治疗癌症方面有用。