BMB Rep. 2016; 49(6): 305-310  
Glycogen synthase kinase 3β in Toll-like receptor signaling
Ryeojin Ko & Soo Young Lee*
Department of Life Science and the Research Center for Cellular Homeostasis, Ewha Womans University, Seoul 03760, Korea
Correspondence to: Tel: +82-2-3277-3770; Fax: +82-2-3277-3760; E-mail: leesy@ewha.ac.kr
Received: March 18, 2016; Published online: June 30, 2016.
© Korean Society for Biochemistry and Molecular Biology. All rights reserved.

Abstract
Toll-like receptors (TLRs) play a critical role in the innate immune response against pathogens. Each TLR recognizes specific pathogen-associated molecular patterns, after which they activate the adaptor protein MyD88 or TRIF-assembled signaling complex to produce immune mediators, including inflammatory cytokines and type I IFNs. Although the activation of TLR is important for host defense, its uncontrolled activation can damage the host. During the past decade, numerous studies have demonstrated that GSK3β is a key regulator of inflammatory cytokine production in MyD88- mediated TLR signaling via TLR2 and TLR4. Recently, GSK3β has also been implicated in the TRIF-dependent signaling pathway via TLR3. In this review, we describe current advances on the regulatory role of GSK3β in immune responses associated with various TLRs. A better understanding of the role of GSK3β in TLR signaling might lead to more effective anti-inflammatory interventions.
Keywords: Glycogen synthase kinase 3β (GSK3β), Inflammatory cytokines, Toll-like receptor (TLR), Type I interferons (IFNs)


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