IL-10 inhibits the starvation induced autophagy in macrophages via class I phosphatidylinositol 3-kinase (PI3K) pathway.

Abstract

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.

• Authors: Hun-Jung Park, Suk Jun Lee, Sang-Hoon Kim, Jihye Han, Joonbeom Bae, Sang Joon Kim, Chung-Gyu Park, Taehoon Chun
• Journal: Molecular immunology (Mol Immunol) Vol. 48 Issue 4 Pg. 720-7 (Jan 2011) ISSN: 1872-9142 [Electronic] England
• PMID: 21095008 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Copyright © 2010 Elsevier Ltd. All rights reserved.

Chemical References

• Multiprotein Complexes
• Proteins
• Receptors, Interleukin-10
• Interleukin-10
• Class I Phosphatidylinositol 3-Kinases
• Mechanistic Target of Rapamycin Complex 1
• Proto-Oncogene Proteins c-akt
• TOR Serine-Threonine Kinases

Topics

• Animals
• Autophagy (drug effects)
• Cell Line
• Class I Phosphatidylinositol 3-Kinases (metabolism)
• Gene Expression Regulation (drug effects)
• Interleukin-10 (pharmacology)
• Macrophages (cytology, drug effects, enzymology)
• Mechanistic Target of Rapamycin Complex 1
• Mice
• Models, Immunological
• Multiprotein Complexes
• Proteins (metabolism)
• Proto-Oncogene Proteins c-akt (metabolism)
• Receptors, Interleukin-10 (genetics, metabolism)
• Signal Transduction (drug effects)
• TOR Serine-Threonine Kinases