Ample evidence exists for activation of invariant natural killer T (iNKT) cells in a sterile manner by endogenous ligands or microbial antigens from the commensal flora, indicating that iNKT cells are not truly self-tolerant. Their controlled autoreactivity state is disturbed in many types of sterile inflammatory disease, resulting in their central role in modulating autoimmune responses. This review focuses on sterile iNKT-cell responses that are initiated by metabolic triggers, such as obesity-associated inflammation and fatty liver disease, as a manifestation of metabolic disease and dyslipidemia, as well as ischemia reperfusion injuries and sickle cell disease, characterized by acute lack of oxygen and oxidative stress response on reperfusion. In the intestine, inflammation and iNKT-cell response type are shaped by the microbiome as an extended "self". Disease- and organ-specific differences in iNKT-cell response type are summarized and help to define common pathways that shape iNKT-cell responses in the absence of exogenous antigen.

中文翻译：

---

无菌性自身炎症性疾病期间不变的自然杀伤 T 细胞激活的代谢触发因素

大量证据表明，内源性配体或来自共生菌群的微生物抗原以无菌方式激活不变的自然杀伤 T ( i NKT) 细胞，表明i NKT 细胞并不是真正的自我耐受。它们受控的自身反应状态在许多类型的无菌炎性疾病中受到干扰，导致它们在调节自身免疫反应中发挥核心作用。本评论重点关注无菌i由代谢触发物（如肥胖相关炎症和脂肪肝疾病）引发的 NKT 细胞反应，作为代谢疾病和血脂异常的表现，以及缺血再灌注损伤和镰状细胞病，其特征是急性缺氧和氧化再灌注应激反应。在肠中，炎症和我NKT细胞响应类型是由微生物作为扩展“自我”形的。在疾病-和器官特异性差异我NKT细胞响应类型进行了总结和帮助确定共同途径该形状我在不存在外源性抗原的NKT细胞应答。