Park Yoon Jeong, Park Jeu, Huh Jin Young, Hwang Injae, Choe Sung Sik, Kim Jae Bum
Department of Biological Sciences, Center for Adipose Tissue Remodeling, College of Natural Sciences, Institute of Molecular Biology and Genetics, Seoul National University, Seoul, South Korea.
Department of Biophysics and Chemical Biology, Seoul National University, Seoul, South Korea.
Front Immunol. 2018 Jun 11;9:1311. doi: 10.3389/fimmu.2018.01311. eCollection 2018.
Adipose tissue is a metabolic organ that plays a central role in controlling systemic energy homeostasis. Compelling evidence indicates that immune system is closely linked to healthy physiologic functions and pathologic dysfunction of adipose tissue. In obesity, the accumulation of pro-inflammatory responses in adipose tissue subsequently leads to dysfunction of adipose tissue as well as whole body energy homeostasis. Simultaneously, adipose tissue also activates anti-inflammatory responses in an effort to reduce the unfavorable effects of pro-inflammation. Notably, the interplay between adipocytes and resident invariant natural killer T (iNKT) cells is a major component of defensive mechanisms of adipose tissue. iNKT cells are leukocytes that recognize lipids loaded on CD1d as antigens, whereas most other immune cells are activated by peptide antigens. In adipose tissue, adipocytes directly interact with iNKT cells by presenting lipid antigens and stimulate iNKT cell activation to alleviate pro-inflammation. In this review, we provide an overview of the molecular and cellular determinants of obesity-induced adipose tissue inflammation. Specifically, we focus on the roles of iNKT cell-adipocyte interaction in maintaining adipose tissue homeostasis as well as the consequent modulation in systemic energy metabolism. We also briefly discuss future research directions regarding the interplay between adipocytes and adipose iNKT cells in adipose tissue inflammation.
脂肪组织是一个在控制全身能量稳态中起核心作用的代谢器官。有力证据表明，免疫系统与脂肪组织的健康生理功能和病理功能障碍密切相关。在肥胖状态下，脂肪组织中促炎反应的积累随后会导致脂肪组织功能障碍以及全身能量稳态失衡。同时，脂肪组织也会激活抗炎反应，以减轻促炎反应的不利影响。值得注意的是，脂肪细胞与驻留的不变自然杀伤T（iNKT）细胞之间的相互作用是脂肪组织防御机制的主要组成部分。iNKT细胞是一种白细胞，它将加载在CD1d上的脂质识别为抗原，而大多数其他免疫细胞则由肽抗原激活。在脂肪组织中，脂肪细胞通过呈递脂质抗原直接与iNKT细胞相互作用，并刺激iNKT细胞活化以减轻促炎反应。在这篇综述中，我们概述了肥胖诱导的脂肪组织炎症的分子和细胞决定因素。具体而言，我们重点关注iNKT细胞与脂肪细胞相互作用在维持脂肪组织稳态以及随后对全身能量代谢的调节中的作用。我们还简要讨论了关于脂肪组织炎症中脂肪细胞与脂肪组织iNKT细胞之间相互作用的未来研究方向。
