Leishmaniasis is an immunosuppressive disease caused by protozoa of the genus Leishmania, for which dogs are the domestic reservoir. The programmed cell death-1 molecule (PD-1) is highly expressed in leukocyte cells of dogs with leishmaniasis, and it promotes T lymphocyte exhaustion and suppression of cytokine secretion. Because PD-1 has a suppressive function regarding cell immunity, we evaluated the effect of PD-1 blocking antibodies on NO, ROS and interleukin 17 (IL-17) production and on parasite load in spleen leukocyte cultures from dogs with leishmaniasis. In vitro, PD-1 blocking promoted increased levels of intracellular NO and NO2 and reduced the levels of IL-17 in the culture supernatant, in addition to reducing the parasite load, but it did not change ROS levels. We conclude that PD-1 participates in the regulation of the immune response and that the blocking antibody is effective in restoring host microbicidal activity. This can be investigated in an immunotherapeutic study in the future.

中文翻译：

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PD-1调节利什曼病犬的利什曼活性和IL-17。

利什曼病是一种由利什曼原虫属的原生动物引起的免疫抑制疾病，犬是家畜的宿主。程序性细胞死亡1分子（PD-1）在患有利什曼病的狗的白细胞中高度表达，并促进T淋巴细胞耗竭和细胞因子分泌的抑制。因为PD-1对细胞免疫具有抑制作用，所以我们评估了PD-1阻断抗体对利什曼病犬的脾白细胞培养物中NO，ROS和白介素17（IL-17）产生以及寄生虫负荷的影响。在体外，PD-1阻断促进了细胞内NO和NO2含量的增加，并降低了培养上清液中IL-17的含量，此外还降低了寄生虫负荷，但并未改变ROS含量。我们得出结论，PD-1参与了免疫应答的调节，而阻断抗体可有效恢复宿主的杀微生物活性。将来可以在免疫治疗研究中对此进行研究。