Department of Pharmaceutical Sciences, College of Pharmacy, University of Kentucky, Lexington, KY, United States.
Department of Pharmacology and Nutritional Sciences, Barnstable Brown Diabetes and Obesity Research Center, University of Kentucky, Lexington, KY, United States.
Front Immunol. 2019 Jul 17;10:1587. doi: 10.3389/fimmu.2019.01587. eCollection 2019.
Obesity-associated inflammation stems from a combination of cell-intrinsic changes of individual immune cell subsets and the dynamic crosstalk amongst a broad array of immune cells. Although much of the focus of immune cell contributions to metabolic disease has focused on adipose tissue-associated cells, these potent sources of inflammation inhabit other metabolic regulatory tissues, including liver and gut, and recirculate to promote systemic inflammation and thus obesity comorbidities. Tissue-associated immune cells, especially T cell subpopulations, have become a hotspot of inquiry based on their contributions to obesity, type 2 diabetes, non-alcoholic fatty liver diseases and certain types of cancers. The cell-cell interactions that take place under the stress of obesity are mediated by intracellular contact and cytokine production, and constitute a complicated network that drives the phenotypic alterations of immune cells and perpetuates a feed-forward loop of metabolic decline. Herein we discuss immune cell functions in various tissues and obesity-associated cancers from the viewpoint of inflammation. We also emphasize recent advances in the understanding of crosstalk amongst immune cell subsets under obese conditions, and suggest future directions for focused investigations with clinical relevance.
肥胖相关的炎症源于单个免疫细胞亚群的细胞内在变化，以及广泛的免疫细胞之间的动态串扰。尽管免疫细胞对代谢疾病的贡献主要集中在与脂肪组织相关的细胞上，但这些炎症的潜在来源还存在于其他代谢调节组织中，包括肝脏和肠道，并重新循环以促进全身炎症，从而导致肥胖的合并症。组织相关的免疫细胞，特别是 T 细胞亚群，由于其对肥胖、2 型糖尿病、非酒精性脂肪性肝病和某些类型的癌症的贡献，已成为研究的热点。在肥胖的压力下发生的细胞间相互作用是通过细胞内接触和细胞因子产生来介导的，并构成了一个复杂的网络，驱动免疫细胞的表型改变，并使代谢下降的正反馈循环持续下去。本文从炎症的角度讨论了各种组织和肥胖相关癌症中的免疫细胞功能。我们还强调了肥胖条件下免疫细胞亚群之间串扰的最新研究进展，并为具有临床相关性的重点研究提出了未来的方向。
