NDLI: IFN-Î³ elicits macrophage autophagy via the p38 MAPK signaling pathway.

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IFN-Î³ elicits macrophage autophagy via the p38 MAPK signaling pathway.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Miyake, Masami Shenoy, Avinash R. Matsuzawa, Takeshi Kim, Bae-Hoon Kamitani, Shigeki Macmicking, John D.
Description	Country affiliation: Japan Author Affiliation: Matsuzawa T ( Osaka Prefecture University, Osaka, Japan. tm@vet.osakafu-u.ac.jp)
Abstract	Autophagy is a major innate immune defense pathway in both plants and animals. In mammals, this cascade can be elicited by cytokines (IFN-Î³) or pattern recognition receptors (TLRs and nucleotide-binding oligomerization domain-like receptors). Many signaling components in TLR- and nucleotide-binding oligomerization domain-like receptor-induced autophagy are now known; however, those involved in activating autophagy via IFN-Î³ remain to be elucidated. In this study, we engineered macrophages encoding a tandem fluorescently tagged LC3b (tfLC3) autophagosome reporter along with stably integrated short hairpin RNAs to demonstrate IFN-Î³-induced autophagy required JAK 1/2, PI3K, and p38 MAPK but not STAT1. Moreover, the autophagy-related guanosine triphosphatase Irgm1 proved dispensable in both stable tfLC3-expressing RAW 264.7 and tfLC3-transduced Irgm1(-/-) primary macrophages, revealing a novel p38 MAPK-dependent, STAT1-independent autophagy pathway that bypasses Irgm1. These unexpected findings have implications for understanding how IFN-Î³-induced autophagy is mobilized within macrophages for inflammation and host defense.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1102041
Journal	The Journal of Immunology
Issue Number	2
Volume Number	189
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2012-07-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Autophagy Immunology Interferon-gamma Physiology Map Kinase Signaling System Macrophages Cytology P38 Mitogen-activated Protein Kinases Animals Genetics Bone Marrow Cells Enzymology Cell Line Gtp-binding Proteins Deficiency Genes, Reporter Mice Mice, Knockout Phagosomes Metabolism Stat1 Transcription Factor Comparative Study Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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