Wang Hao, Li Ming, Zhang Xiaoxia, He Fang, Zhang Shengbin, Zhao Jiaqing
Department of Pathogenic Biology and Medical Immunology, Ningxia Medical University, Yinchuan, Ningxia, China; Key Lab of Hydatid Disease, Ningxia Medical University, Yinchuan, Ningxia, China.
Department of Hepatobiliary Surgery, General Hospital of Ningxia Medical University, Yinchuan, Ningxia, China.
Exp Parasitol. 2017 Mar;174:17-24. doi: 10.1016/j.exppara.2017.01.005. Epub 2017 Jan 31.
Cystic echinococcosis (CE) induced by metacestodes (larval stages) of Echinococcus granulosus (E.granulosus) represents a severe endemic disease worldwide. Gamma delta (γδ) T cells, one of innate immune cells, play pivotal role in pathogenic infections. However, whether γδ T cells are involved in CE remains unclear. This study firstly investigated the role of peripheral γδ T cells in CE. The results showed that the percentage of peripheral γδ T cells from CE patients was decreased, compared with healthy controls (HC) (p < 0.01). This decrease was primarily due to a reduction in Vδ2 subset. Furthermore, Vδ2 T cells in CE expressed lower Natural Killer Group 2D (NKG2D) (p < 0.01). The abundance of Vδ2 T cells correlated negatively with cyst burden. To further identify the function of decreased Vδ2 T cells in CE, proliferation rate, cytokine secretion and cytotoxin were detected subsequently in vitro. As a result, the proliferation rate of Vδ2 cells in CE patients was lower than that in HC (p < 0.01). Meanwhile, Vδ2 T cells from CE patients released significantly decreased interferon (IFN)-γ, compared with HC (p < 0.05). Moreover, the levels of perforin and granzyme B of Vδ2 T cells from the patients were decreased significantly (p < 0.05), suggesting impaired cytotoxin generation of Vδ2 cells in CE. Collectively, our findings indicated that circulating Vδ2 T cells in CE was impaired, and these aberrations may contribute to disease pathogenesis.
由细粒棘球绦虫（E.granulosus）的中绦期（幼虫阶段）引起的囊型棘球蚴病（CE）是一种在全球范围内流行的严重疾病。γδ T细胞作为天然免疫细胞之一，在致病性感染中发挥关键作用。然而，γδ T细胞是否参与CE尚不清楚。本研究首次探讨了外周血γδ T细胞在CE中的作用。结果显示，与健康对照（HC）相比，CE患者外周血γδ T细胞的百分比降低（p < 0.01）。这种降低主要是由于Vδ2亚群减少所致。此外，CE患者的Vδ2 T细胞表达较低水平的自然杀伤细胞2D（NKG2D）（p < 0.01）。Vδ2 T细胞的丰度与囊肿负荷呈负相关。为了进一步确定CE中Vδ2 T细胞减少的功能，随后在体外检测了其增殖率、细胞因子分泌和细胞毒素。结果显示，CE患者Vδ2细胞的增殖率低于HC（p < 0.01）。同时，与HC相比，CE患者的Vδ2 T细胞释放的干扰素（IFN）-γ显著减少（p < 0.05）。此外，患者Vδ2 T细胞的穿孔素和颗粒酶B水平显著降低（p < 0.05），提示CE中Vδ2细胞的细胞毒素生成受损。总体而言，我们的研究结果表明，CE患者循环中的Vδ2 T细胞功能受损，这些异常可能与疾病的发病机制有关。
