Sinton Matthew C, Kajimura Shingo
Division of Immunology, Immunity to Infection and Respiratory Medicine, University of Manchester, UK.
Lydia Becker Institute of Immunology and Inflammation, University of Manchester, UK.
FEBS J. 2025 Apr;292(8):1868-1883. doi: 10.1111/febs.17302. Epub 2024 Oct 20.
Adipose tissue is a rich source of diverse cell populations, including immune cells, adipocytes and stromal cells. Interactions between these different cell types are now appreciated to be critical for maintaining tissue structure and function, by governing processes such as adipogenesis, lipolysis and differentiation of white to beige adipocytes. Interactions between these cells also drive inflammation in obesity, leading to an expansion of adipose tissue immune cells, and the secretion of proinflammatory cytokines from immune cells and from adipocytes themselves. However, in evolutionary terms, obesity is a recent phenomenon, raising the question of why adipocytes evolved to express factors that influence the immune response. Studies of various pathogens indicate that adipocytes are highly responsive to infection, altering their metabolic profiles in a way that can be used to release nutrients and fuel the immune response. In the case of infection with the extracellular parasite Trypanosoma brucei, attenuating the ability of adipocytes to sense the cytokine IL-17 results in a loss of control of the local immune response and an increased pathogen load. Intriguingly, comparisons of the adipocyte response to infection suggest that the immune responses of these cells occur in a pathogen-dependent manner, further confirming their complexity. Here, with a focus on murine adipose tissue, we discuss the emerging concept that, in addition to their canonical function, adipocytes are immune signalling hubs that integrate and disseminate signals from the immune system to generate a local environment conducive to pathogen clearance.
脂肪组织是多种细胞群体的丰富来源，包括免疫细胞、脂肪细胞和基质细胞。现在人们认识到，这些不同细胞类型之间的相互作用对于维持组织结构和功能至关重要，其通过控制脂肪生成、脂肪分解以及白色脂肪细胞向米色脂肪细胞的分化等过程来实现。这些细胞之间的相互作用还会在肥胖状态下引发炎症，导致脂肪组织免疫细胞增多，以及免疫细胞和脂肪细胞自身分泌促炎细胞因子。然而，从进化的角度来看，肥胖是一种近期才出现的现象，这就引发了一个问题：为什么脂肪细胞会进化出表达影响免疫反应的因子的能力。对各种病原体的研究表明，脂肪细胞对感染高度敏感，会以一种可用于释放营养物质并为免疫反应提供燃料的方式改变其代谢特征。在感染细胞外寄生虫布氏锥虫的情况下，削弱脂肪细胞感知细胞因子IL-17的能力会导致局部免疫反应失控以及病原体载量增加。有趣的是，对脂肪细胞感染反应的比较表明，这些细胞的免疫反应以病原体依赖的方式发生，这进一步证实了它们的复杂性。在这里，我们以小鼠脂肪组织为重点，讨论一个新出现的概念，即除了其经典功能外，脂肪细胞还是免疫信号枢纽，整合并传播来自免疫系统的信号，以产生有利于病原体清除的局部环境。
