NDLI: Glia maturation factor-Î³ negatively modulates TLR4 signaling by facilitating TLR4 endocytic trafficking in macrophages.

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Glia maturation factor-Î³ negatively modulates TLR4 signaling by facilitating TLR4 endocytic trafficking in macrophages.

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Glia maturation factor-Î³ negatively modulates TLR4 signaling by facilitating TLR4 endocytic trafficking in macrophages.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Lee, Kevin Chin, Kyung Rodgers, Griffin P. Aerbajinai, Wulin
Description	Country affiliation: United States Author Affiliation: Aerbajinai W ( Molecular and Clinical Hematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA.)
Abstract	TLR4 signaling must be tightly regulated to provide both effective immune protection and avoid inflammation-induced pathology. Thus, the mechanisms that negatively regulate the TLR4-triggered inflammatory response are of particular importance. Glia maturation factor-Î³ (GMFG), a novel actin depolymerization factor/cofilin superfamily protein that is expressed in inflammatory cells, has been implicated in mediating neutrophil and T cell migration, but its function in macrophage immune response remains unclear. In the current study, the role of GMFG in the LPS-induced TLR4-signaling pathway was investigated in THP-1 macrophages and human primary macrophages. LPS stimulation of macrophages decreased GMFG mRNA and protein expression. We show that GMFG negatively regulates LPS-induced activation of NF-κB-, MAPK-, and IRF3-signaling pathways and subsequent production of proinflammatory cytokines and type I IFN in human macrophages. We found that endogenous GMFG localized within early and late endosomes. GMFG knockdown delayed LPS-induced TLR4 internalization and caused prolonged TLR4 retention at the early endosome, suggesting that TLR4 transport from early to late endosomes is interrupted, which may contribute to enhanced LPS-induced TLR4 signaling. Taken together, our findings suggest that GMFG functions as a negative regulator of TLR4 signaling by facilitating TLR4 endocytic trafficking in macrophages.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1203048
Journal	The Journal of Immunology
Issue Number	12
Volume Number	190
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2013-06-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Glia Maturation Factor Metabolism Macrophages Signal Transduction Physiology Toll-like Receptor 4 Flow Cytometry Fluorescent Antibody Technique Immunology Immunoblotting Microscopy, Confocal Polymerase Chain Reaction Protein Transport Rna Interference Research Support, N.i.h., Intramural Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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