Cardiovascular Research Institute, University of California, San Francisco, San Francisco, CA;
Blood. 2013 Nov 7;122(19):3263-7. doi: 10.1182/blood-2013-04-459446. Epub 2013 Sep 24.
The rise of obesity and its attendant pathological sequelae, including type 2 diabetes and coronary artery disease, constitute an ongoing public health catastrophe in both the developed and, more recently, the developing world. Although the underlying pathophysiology is complex, chronic low-grade inflammation has emerged as a central driver of both primary metabolic dysfunction and subsequent tissue failure. Importantly, this inflammation has been shown to arise as a consequence of both the disruption of homeostatic tissue resident leukocytes and the recruitment of antagonistic effector cells from the circulation. In this review, we discuss the roles of visceral adipose tissue's salient leukocyte lineages in the transition to obesity and highlight key points at which this emerging immune axis may be manipulated for therapeutic effect.
肥胖及其伴随的病态后果（包括 2 型糖尿病和冠状动脉疾病）在发达国家和最近的发展中国家都是持续存在的公共卫生灾难。尽管潜在的病理生理学很复杂，但慢性低度炎症已成为原发性代谢功能障碍和随后组织衰竭的主要驱动因素。重要的是，这种炎症是由于稳态组织常驻白细胞的破坏以及来自循环的拮抗效应细胞的募集而产生的。在这篇综述中，我们讨论了内脏脂肪组织中显著的白细胞谱系在向肥胖过渡中的作用，并强调了这个新兴免疫轴可能被用于治疗效果的关键要点。
