Sensing of Viral Infection and Activation of Innate Immunity by Toll-Like Receptor 3

Abstract

SUMMARY Toll-like receptors (TLRs) form a major group of transmembrane receptors that are involved in the detection of invading pathogens. Double-stranded RNA is a marker for viral infection that is recognized by TLR3. TLR3 triggering activates specific signaling pathways that culminate in the activation of NF-κB and IRF3 transcription factors, as well as apoptosis, enabling the host to mount an effective innate immune response through the induction of cytokines, chemokines, and other proinflammatory mediators. In this review, we describe the paradoxical role of TLR3 in innate immunity against different viruses and in viral pathogenesis but also the evidence for TLR3 as a “danger” receptor in nonviral diseases. We also discuss the structure and cellular localization of TLR3, as well as the complex signaling and regulatory events that contribute to TLR3-mediated immune responses.

Genomic organization and expression analysis of Toll-like receptor 3 in grass carp (Ctenopharyngodon idella)

“…Double-stranded RNA is a marker for viral infection that is recognized by TLR3 [2]. TLR3 triggers specific signaling pathways that culminate in the activation of NF-kB and IRF3 transcription factors, as well as apoptosis, enabling the host to mount an effective innate immune response through the induction of cytokines, chemokines, and other proinflammatory mediators [3,4]. The adjuvant role of poly I:C also requires TLR3 [5].…”

Isolation and expression of grass carp toll-like receptor 5a (CiTLR5a) and 5b (CiTLR5b) gene involved in the response to flagellin stimulation and grass carp reovirus infection

“…GCRV belongs to the Reoviridae family, which contains doublestrands RNA and two capsid layers [24]. In TLRs, the recognition of double-strands RNA was mediated by TLR3, which activated the NF-kB and other downstream genes via the MyD88-independent signaling pathway [25,26]. In our study, the up-regulation of TLR5s and their downstream genes may be due to the signaling feedback system.…”

Progress and prospects: Immunobiology of gene therapy for neurodegenerative disease: prospects and risks

“…10,19 Envelope glycoproteins of HSV activate cytokine responses through TLR2. TLR9 recognizes unmethylated CpG DNA motifs present in the adenovirus genome and responds to Immunobiology of gene therapy for neurodegenerative disease MM McMenamin and MJA Wood ligation by increasing pro-inflammatory cytokine secretion.…”

“…7 Perhaps surprisingly, all CNS cell types, including neurons, express these receptors and their ligation is important in regulating immune privilege as it enables a rapid response to infection, and provides a critical link between innate and adaptive immunity. [8][9][10][11][12] After activation of these receptors, the release of pro-inflammatory cytokines and chemokines activates the adaptive immune response. 13 The adaptive immune response involves interaction of T-cell receptors with antigen in the context of MHC molecule-peptide complexes in the nanometer scale gap between T cells and APCs, referred to as an immunological synapse.…”