Department of Biomedical Sciences, Faculty of Medicine, Prince of Songkla University, Songkhla 90110, Thailand.
Tumor Biology Research Unit, Department of Surgery, Faculty of Medicine, Prince of Songkla University, Songkhla 90110, Thailand.
Mol Med Rep. 2018 Jan;17(1):1403-1412. doi: 10.3892/mmr.2017.8038. Epub 2017 Nov 13.
The immune system has previously been demonstrated to be associated with the pathophysiological development of metabolic abnormalities. However, the mechanisms linking immunity to metabolic disease remain to be fully elucidated. It has previously been suggested that innate lymphoid cells (ILCs) may be involved in the progression of numerous types of metabolic diseases as these cells act as suppressors and promoters for obesity and associated conditions, and are particularly involved in adipose tissue inflammation, which is a major feature of metabolic imbalance. Group 2 ILCs (ILC2s) have been revealed as anti‑obese immune regulators by secreting anti‑inflammatory cytokines and promoting the polarization of M2 macrophages, whereas group 1 ILCs (ILC1s), including natural killer cells, may promote adipose tissue inflammation via production of interferon‑γ, which in turn polarizes macrophages toward the M1 type. The majority of studies to date have demonstrated the pathological association between ILCs and obesity in the context of adipose tissue inflammation, whereas the roles of ILCs in other organs which participate in obesity development have not been fully characterized. Therefore, identifying the roles of all types of ILCs as central components mediating obesity‑associated inflammation, is of primary concern, and may lead to the discovery of novel preventative and therapeutic interventions.
免疫系统先前已被证明与代谢异常的病理生理发展有关。然而,将免疫与代谢疾病联系起来的机制仍有待充分阐明。先前有人提出,固有淋巴细胞(ILC)可能参与多种代谢疾病的进展,因为这些细胞作为肥胖及其相关病症的抑制物和促进物,特别参与脂肪组织炎症,这是代谢失衡的主要特征。第 2 组固有淋巴细胞(ILC2)通过分泌抗炎细胞因子和促进 M2 巨噬细胞的极化,被揭示为抗肥胖的免疫调节剂,而包括自然杀伤细胞在内的第 1 组固有淋巴细胞(ILC1)则可能通过产生干扰素-γ促进脂肪组织炎症,进而将巨噬细胞向 M1 型极化。迄今为止的大多数研究表明,在脂肪组织炎症的背景下,ILC 与肥胖之间存在病理性关联,而 ILC 在参与肥胖发展的其他器官中的作用尚未得到充分表征。因此,确定所有类型的 ILC 作为介导肥胖相关炎症的核心组成部分的作用是首要关注的问题,这可能导致发现新的预防和治疗干预措施。