Department of Parasitology, National Institute of Infectious Disease, Tokyo, 162-8640, Japan.
Department of Parasitology, Graduate School of Medicine, Gunma University, Maebashi, 371-8511, Japan.
Nat Commun. 2020 Apr 22;11(1):1922. doi: 10.1038/s41467-020-15857-x.
Type 1 diabetes (T1D) is an autoimmune disease in which insulin-producing pancreatic β-cells are destroyed. Intestinal helminths can cause asymptomatic chronic and immunosuppressive infections and suppress disease in rodent models of T1D. However, the underlying regulatory mechanisms for this protection are unclear. Here, we report that CD8 regulatory T (Treg) cells prevent the onset of streptozotocin -induced diabetes by a rodent intestinal nematode. Trehalose derived from nematodes affects the intestinal microbiota and increases the abundance of Ruminococcus spp., resulting in the induction of CD8 Treg cells. Furthermore, trehalose has therapeutic effects on both streptozotocin-induced diabetes and in the NOD mouse model of T1D. In addition, compared with healthy volunteers, patients with T1D have fewer CD8 Treg cells, and the abundance of intestinal Ruminococcus positively correlates with the number of CD8 Treg cells in humans.
1 型糖尿病（T1D）是一种自身免疫性疾病，其中产生胰岛素的胰腺β细胞被破坏。肠道寄生虫可以引起无症状的慢性和免疫抑制性感染，并抑制 T1D 啮齿动物模型中的疾病。然而，这种保护的潜在调节机制尚不清楚。在这里，我们报告说，CD8 调节性 T（Treg）细胞通过啮齿动物肠道线虫来预防链脲佐菌素诱导的糖尿病的发生。来源于线虫的海藻糖会影响肠道微生物群，并增加 Ruminococcus spp 的丰度，从而诱导 CD8 Treg 细胞。此外，海藻糖对链脲佐菌素诱导的糖尿病和 T1D 的 NOD 小鼠模型均具有治疗作用。另外，与健康志愿者相比，1 型糖尿病患者的 CD8 Treg 细胞较少，而肠道 Ruminococcus 的丰度与人类的 CD8 Treg 细胞数量呈正相关。
Zotero 插件