College of Life Sciences and Biotechnology, Korea University, Seoul 136-701, Republic of Korea.
Mol Immunol. 2011 Jan;48(4):720-7. doi: 10.1016/j.molimm.2010.10.020. Epub 2010 Nov 20.
Autophagy is an important process which maintains cellular homeostasis under stressful conditions such as starvation and pathogenic invasion. Previous observations have indicated that several cytokines are important regulators of the autophagic process. Among the various cytokines, IL-10 has a unique property which functions to suppress overall immunity. However, the functional role of IL-10 during the autophagic process has not been studied. In this study, we examined the effect of IL-10 during starvation induced autophagy of murine macrophages (J774). The results clearly indicated that IL-10 and IL-10 receptor signaling inhibits autophagy induction of murine macrophage. Further experiments revealed that IL-10 activates the class I phosphatidylinositol 3-kinase (PI3K) pathway, which results in the phosphorylation of p70S6K through the activation of Akt and a mammalian target of the rapamycin complex 1 (mTORC 1). These results will advance our understanding of the physiological function of IL-10 during the autophagic process of macrophage.
自噬是一种重要的过程，可在饥饿和病原入侵等应激条件下维持细胞内稳态。先前的观察表明，几种细胞因子是自噬过程的重要调节剂。在各种细胞因子中，IL-10 具有独特的特性，可起到抑制整体免疫的作用。然而，IL-10 在自噬过程中的功能作用尚未得到研究。在这项研究中，我们研究了 IL-10 在饥饿诱导的鼠巨噬细胞（J774）自噬中的作用。结果清楚地表明，IL-10 和 IL-10 受体信号抑制了鼠巨噬细胞的自噬诱导。进一步的实验表明，IL-10 激活了 I 类磷脂酰肌醇 3-激酶（PI3K）途径，通过 Akt 和雷帕霉素复合物 1（mTORC1）的激活，导致 p70S6K 的磷酸化。这些结果将增进我们对 IL-10 在巨噬细胞自噬过程中的生理功能的理解。
