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.
Original language | English |
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Pages (from-to) | 305-310 |
Number of pages | 6 |
Journal | BMB Reports |
Volume | 49 |
Issue number | 6 |
DOIs | |
State | Published - 2016 |
Bibliographical note
Publisher Copyright:© 2016 by the The Korean Society for Biochemistry and Molecular Biology.
Keywords
- Glycogen synthase kinase 3β (GSK3β
- Inflammatory cytokines
- Toll-like receptor (TLR)
- Type I interferons (IFNs)