Paz-Filho Gilberto, Mastronardi Claudio, Franco Carina Bertoldi, Wang Kevin Boyang, Wong Ma-Li, Licinio Julio
Australian National University, Canberra, Australia.
Arq Bras Endocrinol Metabol. 2012 Dec;56(9):597-607. doi: 10.1590/s0004-27302012000900001.
Leptin, the adipokine produced mainly by the white adipose tissue, plays important roles not only in the regulation of food intake, but also in controlling immunity and inflammation. It has been widely demonstrated that the absence of leptin leads to immune defects in animal and human models, ultimately increasing mortality. Leptin also regulates inflammation by means of actions on its receptor, that is widely spread across different immune cell populations. The molecular mechanisms by which leptin determines its biological actions have also been recently elucidated, and three intracellular pathways have been implicated in leptin actions: JAK-STAT, PI3K, and ERK 1/2. These pathways are closely regulated by intracellular proteins that decrease leptin biological activity. In this review, we discuss the molecular mechanisms by which leptin regulates immunity and inflammation, and associate those mechanisms with chronic inflammatory disorders.
瘦素是主要由白色脂肪组织产生的脂肪因子，不仅在食物摄入调节中发挥重要作用，还在控制免疫和炎症方面发挥作用。大量研究表明，在动物和人类模型中，缺乏瘦素会导致免疫缺陷，最终增加死亡率。瘦素还通过作用于其受体来调节炎症，该受体广泛分布于不同的免疫细胞群体中。最近，瘦素发挥其生物学作用的分子机制也已阐明，并且有三条细胞内途径与瘦素作用有关：JAK-STAT、PI3K和ERK 1/2。这些途径受到降低瘦素生物学活性的细胞内蛋白质的密切调节。在这篇综述中，我们讨论了瘦素调节免疫和炎症的分子机制，并将这些机制与慢性炎症性疾病联系起来。
