Abstract

Simple SummaryThe gypsy moth, Lymantria dispar is one of the main forest defoliators worldwide. The baculovirus, Lymantria dispar multiple nucleopolyhedrovirus (LdMNPV), can naturally control this pest and is safe to non-target organisms. However, Toll-like receptor (TLR) signaling pathway, which plays a critical role in innate immunity both in vertebrates and invertebrates, and its underlying immune mechanism against LdMNPV invasion in L. dispar have not been investigated. In this study, eleven TLRs and five downstream TLR pathway components of L. dispar were identified. All of these proteins comprised typical domain architecture. Primary and tertiary structure analysis revealed that Toll/interleukin-1 receptor (TIR) domains of TLRs from L. dispar were conserved during evolution. Expression analysis showed that several TLRs and all identified downstream genes of TLR pathway in L. dispar were significantly up-regulated in response to LdMNPV infection, implying that the TLR pathway of L. dispar was activated and may be involved in L. dispar innate immunity against LdMNPV infection. Taken together, this research contributed to the clarification of innate immunity in L. dispar.The gypsy moth, Lymantria dispar, is a polyphagous forest pest worldwide. The baculovirus, Lymantria dispar multiple nucleopolyhedrovirus (LdMNPV) is a natural pathogen of L. dispar. The Toll-like receptors (TLR) pathway plays a crucial role in both innate and adaptive immunity in animals. However, The TLR pathway and its underlying immune mechanism against baculovirus in L. dispar have not been explored. In this study, eleven TLRs and five downstream TLR pathway components were identified and characterized from L. dispar. Structural analysis indicated that intracellular Toll/interleukin-1 receptor (TIR) domains of LdTLRs and LdMyD88 contained three conserved motifs, and the 3D structures of TIR domains of LdTLRs possessed similar patterns in components arrangement and spatial conformation. The TLR proteins of L. dispar were placed into five monophyletic groups based on the phylogenetic analysis. LdTLR1, 2, 5, 6, 7, 8 and all identified downstream TLR pathway factors were highly induced upon LdMNPV infection, indicating that the TLR pathway of L. dispar was activated and might play a role in the immune response to LdMNPV infection. Collectively, these results help elucidate the crucial role of the TLR pathway in the immune response of L. dispar against LdMNPV, and offer a foundation for further understanding of innate immunity of the pest.

Highlights

  • For multicellular animals, innate immunity is an efficient first line of defense to avoid pathogen invasion and activate different signaling pathways [1]

  • The innate immune system is characterized by the activation of various pattern recognition receptors (PRRs) responsible for recognizing various pathogen-associated molecular pattern (PAMP), molecules present in the pathogen but not found in the host [3]

  • Few Toll-like receptors (TLR) have been described in L. dispar and their immune function role in response to baculovirus challenge was still obscure

Read more

Summary

Introduction

Innate immunity is an efficient first line of defense to avoid pathogen invasion and activate different signaling pathways [1]. Invertebrates, such as insects, lack an adaptive immune system and mainly depend on the innate immune system to counter the diverse pathogens that include fungi, bacteria and viruses [2]. There are three signaling pathways in insect immune responses, including the Toll (or Toll-like receptor, TLR) pathway, immune deficiency (Imd) pathway and Janus kinase signal transducer and activator of transcription (JAK/STAT) pathway [4]. The JAK/STAT pathway is multi-functional, controlling immune-regulatory functions and other biological activities such as cell proliferation, differentiation and apoptosis functions [6]

Methods
Results
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call