Toll-Like Receptors (TLRs), NOD-Like Receptors (NLRs), and RIG-I-Like Receptors (RLRs) in Innate Immunity. TLRs, NLRs, and RLRs Ligands as Immunotherapeutic Agents for Hematopoietic Diseases

Wicherska‐Pawłowska, Katarzyna; Wróbel, Tomasz; Rybka, Justyna

doi:10.3390/ijms222413397

Cited by 154 publications

(85 citation statements)

References 184 publications

(236 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This process subsequently alerts neighboring immune cells to viral infections encountered. Pattern-recognition receptors (PRRs), including toll like receptors (TLRs), NOD-like receptors (NOD-like receptors, NLRs) and RIG-I like receptors (RLRs) ( 15 ), which specifically recognize the PAMP. The RLRs are a class of RNA helicases (containing DEX/DH box) that recognize virus-derived double strand RNA (dsRNA) and produce type I interferons (IFN-α and IFN-β) upon virus infection ( 16 ).…”

Section: Rig-i Signaling Pathway: a Brief Overviewmentioning

confidence: 99%

Endothelial Cells as a Key Cell Type for Innate Immunity: A Focused Review on RIG-I Signaling Pathway

Jin

Weng

2022

Front. Immunol.

View full text Add to dashboard Cite

The vascular endothelium consists of a highly heterogeneous monolayer of endothelial cells (ECs) which are the primary target for bacterial and viral infections due to EC’s constant and close contact with the bloodstream. Emerging evidence has shown that ECs are a key cell type for innate immunity. Like macrophages, ECs serve as sentinels when sensing invading pathogens or microbial infection caused by viruses and bacteria. It remains elusive how ECs senses danger signals, transduce the signal and fulfil immune functions. Retinoic acid-inducible gene-I (RIG-I, gene name also known as DDX58) is an important member of RIG-I-like receptor (RLR) family that functions as an important pathogen recognition receptor (PRR) to execute immune surveillance and confer host antiviral response. Recent studies have demonstrated that virus infection, dsRNA, dsDNA, interferons, LPS, and 25-hydroxycholesterol (25-HC) can increase RIG-1 expression in ECs and propagate anti-viral response. Of translational significance, RIG-I activation can be inhibited by Panax notoginseng saponins, endogenous PPARγ ligand 15-PGJ2, tryptanthrin and 2-animopurine. Considering the pivotal role of inflammation and innate immunity in regulating endothelial dysfunction and atherosclerosis, here we provided a concise review of the role of RIG-I in endothelial cell function and highlight future direction to elucidate the potential role of RIG-I in regulating cardiovascular diseases as well as virus infectious disease, including COVID-19. Furthered understanding of RIG-I-mediated signaling pathways is important to control disorders associated with altered immunity and inflammation in ECs.

show abstract

Section: Rig-i Signaling Pathway: a Brief Overviewmentioning

confidence: 99%

Endothelial Cells as a Key Cell Type for Innate Immunity: A Focused Review on RIG-I Signaling Pathway

Jin

Weng

2022

Front. Immunol.

View full text Add to dashboard Cite

show abstract

“…The ultimate action of PRR signal transduction cascades is the activation and translocation to the nucleus of prosurvival/pro-inflammatory transcription factors NFkB and AP-1 and interferon (IFN) regulatory factors (IRFs) [65].…”

Section: Transcription Factorsmentioning

confidence: 99%

In search of the Aplysia immunome: an in silico study

Kron

2022

BMC Genomics

View full text Add to dashboard Cite

The immune repertoires of mollusks beyond commercially important organisms such as the pacific oyster Crassostrea gigas or vectors for human pathogens like the bloodfluke planorb Biomphalaria glabrata are understudied. Despite being an important model for neural aging and the role of inflammation in neuropathic pain, the immune repertoire of Aplysia californica is poorly understood. Recent discovery of a neurotropic nidovirus in Aplysia has highlighted the need for a better understanding of the Aplysia immunome. To address this gap in the literature, the Aplysia reference genome was mined using InterProScan and OrthoFinder for putative immune genes. The Aplysia genome encodes orthologs of all critical components of the classical Toll-like receptor (TLR) signaling pathway. The presence of many more TLRs and TLR associated adapters than known from vertebrates suggest yet uncharacterized, novel TLR associated signaling pathways. Aplysia also retains many nucleotide receptors and antiviral effectors known to play a key role in viral defense in vertebrates. However, the absence of key antiviral signaling adapters MAVS and STING in the Aplysia genome suggests divergence from vertebrates and bivalves in these pathways. The resulting immune gene set of this in silico study provides a basis for interpretation of future immune studies in this important model organism.

show abstract

“…Several classes of pattern-associated molecular patterns (PRRs), including TLRs, Nucleotide-binding oligomerization domain-like receptors (NLRs) and Retinoicacid-inducible gene-like receptors (RLRs) recognize distinct microbial components and directly activate immune cells ( Wicherska-Pawłowska et al., 2021 ). TLRs are transmembrane receptors, while NLRs and RLRs are intracellular molecules.…”

Section: Introductionmentioning

confidence: 99%

Toll-Like Receptor 2 Modulates Pulmonary Inflammation and TNF-α Release Mediated by Mycoplasma pneumoniae

Chen

Deng

Zhao

et al. 2022

Front. Cell. Infect. Microbiol.

View full text Add to dashboard Cite

ObjectivesTo investigate the roles that Toll-like receptors (TLRs) play in lung inflammation mediated by Mycoplasma pneumoniae (MP).MethodsThe changes in TLRs and tumor necrosis factor alpha (TNF-α) in peripheral blood of children with M. pneumoniae pneumonia (MPP) were monitored, and the interactions of signaling molecules regulating TNF-α release in A549 cells and neutrophils after M. pneumoniae stimulation were investigated. In TLR2 knockout (TLR2-/-) mice, the levels of TNF-α in bronchial alveolar lavage fluid (BALF) and peripheral blood after mycoplasma infection and the pathological changes in the lung tissue of mice were detected.ResultsTNF-α levels in peripheral blood of children with MPP were higher than those in non-infected children, and children with refractory MPP had the highest levels of TNF-α and TLR2. TNF-α secretion and TLR2, myeloid differentiation primary response 88 (MyD88) and phospho-p65(p-p65) levels were increased in stimulated cells. TNF-α secretion was suppressed upon siRNA-mediated TLR2 silencing. Pharmacological inhibition of nuclear factor-kappa B (NF-κB) and MyD88 effectively reduced TNF-α expression. Compared with wild-type mice, the TNF-α in serum and BALF decreased, and lung pro-inflammatory response was partially suppressed in TLR2-/- mice.ConclusionWe concluded that TLR2 regulates M. pneumoniae-mediated lung inflammation and TNF-α release through the TLR2-MyD88-NF-κB signaling pathway.

show abstract

Toll-Like Receptors (TLRs), NOD-Like Receptors (NLRs), and RIG-I-Like Receptors (RLRs) in Innate Immunity. TLRs, NLRs, and RLRs Ligands as Immunotherapeutic Agents for Hematopoietic Diseases

Cited by 154 publications

References 184 publications

Endothelial Cells as a Key Cell Type for Innate Immunity: A Focused Review on RIG-I Signaling Pathway

Endothelial Cells as a Key Cell Type for Innate Immunity: A Focused Review on RIG-I Signaling Pathway

In search of the Aplysia immunome: an in silico study

Toll-Like Receptor 2 Modulates Pulmonary Inflammation and TNF-α Release Mediated by Mycoplasma pneumoniae

Contact Info

Product

Resources

About