Abstract
Toll-Like Receptors (TLRs) are membrane-bound proteins that recognize invading organisms with Pathogen-Associated Molecular Patterns (PAMPs) and Damage-Related Molecular Patterns (DAMPs)...
Highlights
Toll-Like Receptors (TLRs) are membrane-bound proteins that recognize invading organisms with Pathogen-Associated Molecular Patterns (PAMPs) and Damage-Related Molecular Patterns (DAMPs) [1]
These results suggested that Toll-Like Receptor 4 (TLR4), myeloid differentiation primary response gene 88 (MyD88) and Interleukin-1 Receptor-Associated Kinase 4 (IRAK4) might participate in the skin immune system of Rana dybowskii during the breeding and pre-hibernation periods
The present results demonstrated that TLR4, MyD88 and IRAK4 were localized in epithelial and gland cells of the skin of Rana dybowskii in the breeding and pre-hibernation periods
Summary
Toll-Like Receptors (TLRs) are membrane-bound proteins that recognize invading organisms with Pathogen-Associated Molecular Patterns (PAMPs) and Damage-Related Molecular Patterns (DAMPs) [1]. TLRs activated by PAMP or DAMP could upregulate chemokines and inflammatory cytokines and participate in various intracellular signaling pathways to regulate the inflammatory responses (Brown et al, 2011). TLR4, the first TLR to be identified by Medzhitov in 1997, is the only receptor that mediates the immune response through the MyD88-dependent signaling pathway and the MyD88independent signaling pathway and is a key component of the innate immune system [2]. TLR4 recruit’s adaptor proteins such as MyD88 to IRAK4 and TNF receptor associated factor 6 (TRAF6), induces the activation of COX2, which plays a key regulatory role in skin inflammation Sherwani (2018). MyD88 is an adaptor protein for most TLR signaling pathways in regulation of the innate immunity [4]. The main function of the skin immune system is to promote wound healing and immune tolerance [10]
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