Department of Medical Biochemistry, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands.
Department of Clinical Pathobiochemistry, Department of Medicine, Institute for Clinical Chemistry and Laboratory Medicine, and Paul-Langerhans-Institute, Technische Universität Dresden, Dresden, Germany.
Diabetes. 2014 Dec;63(12):3982-91. doi: 10.2337/db14-0272.
In the past two decades, numerous experimental and clinical studies have established the importance of inflammation and immunity in the development of obesity and its metabolic complications, including insulin resistance and type 2 diabetes mellitus. In this context, T cells orchestrate inflammatory processes in metabolic organs, such as the adipose tissue (AT) and liver, thereby mediating obesity-related metabolic deterioration. Costimulatory molecules, which are present on antigen-presenting cells and naïve T cells in the AT, are known to mediate the crosstalk between the adaptive and innate immune system and to direct T-cell responses in inflammation. In this Perspectives in Diabetes article, we highlight the newest insights in immune cell interactions in obesity and discuss the role of costimulatory dyads in its pathogenesis. Moreover, the potential of therapeutic strategies that target costimulatory molecules in the metabolic syndrome is explored.
在过去的二十年中,大量的实验和临床研究已经确立了炎症和免疫在肥胖及其代谢并发症(包括胰岛素抵抗和 2 型糖尿病)发展中的重要性。在这种情况下,T 细胞在代谢器官(如脂肪组织 [AT] 和肝脏)中协调炎症过程,从而介导肥胖相关的代谢恶化。已知存在于 AT 中的抗原呈递细胞和初始 T 细胞上的共刺激分子介导适应性和固有免疫系统之间的串扰,并指导炎症中的 T 细胞反应。在这篇糖尿病观点文章中,我们强调了肥胖症中免疫细胞相互作用的最新见解,并讨论了共刺激二联体在其发病机制中的作用。此外,还探讨了靶向代谢综合征中共刺激分子的治疗策略的潜力。