Glycogen synthase kinase 3β in Toll-like receptor signaling

Ryeojin Ko, Soo Young Lee

Research output: Contribution to journalReview articlepeer-review

43 Scopus citations


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 languageEnglish
Pages (from-to)305-310
Number of pages6
JournalBMB Reports
Issue number6
StatePublished - 2016

Bibliographical note

Publisher Copyright:
© 2016 by the The Korean Society for Biochemistry and Molecular Biology.


  • Glycogen synthase kinase 3β (GSK3β
  • Inflammatory cytokines
  • Toll-like receptor (TLR)
  • Type I interferons (IFNs)


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