TLR10: An intriguing Toll-like receptor with many unanswered questions

Rodrigues, Carolina Rego; Balachandran, Yadu; Aulakh, Gurpreet Kaur; Singh, Baljit

doi:10.1159/000535523

Cited by 2 publications

(2 citation statements)

References 62 publications

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“…TLR13 is specific for rRNA regions, particularly certain 23S rRNA motifs found in bacteria [105,106]. Human TLR10 has been shown to bind to dsRNA in vitro at acidic pH, suggesting it has an endosomal location [107] in addition to having a plasma membrane localization [108]. The exact mechanisms of TLR10 are somewhat unclear and it is suspected to have both pro-and anti-inflammatory properties (reviewed in [108]).…”

Section: Tlr Signaling In Sle-an Update On Recent Findingsmentioning

confidence: 99%

“…Human TLR10 has been shown to bind to dsRNA in vitro at acidic pH, suggesting it has an endosomal location [107] in addition to having a plasma membrane localization [108]. The exact mechanisms of TLR10 are somewhat unclear and it is suspected to have both pro-and anti-inflammatory properties (reviewed in [108]). Interestingly, in relation to SLE, Lee et al (2018) showed that the binding of TLR10 to dsRNA activated the MyD88 signaling pathway and suppression of IRF7-dependent type I IFN expression as well as inhibition of TLR3 signaling through sequestering dsRNA from this receptor [107].…”

Section: Tlr Signaling In Sle-an Update On Recent Findingsmentioning

confidence: 99%

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Human and Murine Toll-like Receptor-Driven Disease in Systemic Lupus Erythematosus

von Hofsten,

Fenton,

Pedersen

2024

IJMS

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The pathogenesis of systemic lupus erythematosus (SLE) is linked to the differential roles of toll-like receptors (TLRs), particularly TLR7, TLR8, and TLR9. TLR7 overexpression or gene duplication, as seen with the Y-linked autoimmune accelerator (Yaa) locus or TLR7 agonist imiquimod, correlates with increased SLE severity, and specific TLR7 polymorphisms and gain-of-function variants are associated with enhanced SLE susceptibility and severity. In addition, the X-chromosome location of TLR7 and its escape from X-chromosome inactivation provide a genetic basis for female predominance in SLE. The absence of TLR8 and TLR9 have been shown to exacerbate the detrimental effects of TLR7, leading to upregulated TLR7 activity and increased disease severity in mouse models of SLE. The regulatory functions of TLR8 and TLR9 have been proposed to involve competition for the endosomal trafficking chaperone UNC93B1. However, recent evidence implies more direct, regulatory functions of TLR9 on TLR7 activity. The association between age-associated B cells (ABCs) and autoantibody production positions these cells as potential targets for treatment in SLE, but the lack of specific markers necessitates further research for precise therapeutic intervention. Therapeutically, targeting TLRs is a promising strategy for SLE treatment, with drugs like hydroxychloroquine already in clinical use.

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Section: Tlr Signaling In Sle-an Update On Recent Findingsmentioning

confidence: 99%

Section: Tlr Signaling In Sle-an Update On Recent Findingsmentioning

confidence: 99%

Human and Murine Toll-like Receptor-Driven Disease in Systemic Lupus Erythematosus

von Hofsten,

Fenton,

Pedersen

2024

IJMS

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RNA sequencing reveals dynamic expression of genes related to innate immune responses in canine small intestinal epithelial cells induced by Echinococcus granulosus protoscoleces

Wang,

Pu,

Zhao

et al. 2024

Front. Vet. Sci.

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BackgroundDogs are definitive hosts of Echinococcus granulosus, with the small intestine being the only site of parasitic infections. However, the immunomodulatory processes that occur during interactions between E. granulosus and its definitive host remain unclear. Therefore, this study aimed to evaluate gene transcription patterns in canine small intestinal epithelial cells (CIECs) following stimulation by E. granulosus protoscoleces (PSCs). Particularly, this study investigated the roles of pattern recognition receptors (PRRs), involved in recognizing pathogen-associated molecular patterns (PAMPs) and mediating the host innate immune response to the tapeworm E. granulosus.MethodsRNA sequencing (RNA-seq) was used to examine gene transcription patterns in CIECs following stimulation with PSCs for 12 and 24 h. The potential roles of differentially expressed (DE) genes were inferred through Gene Ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses.ResultsRNA-seq analysis identified 78,206,492–90,548,214 clean reads in 12 RNA samples. This included six samples stimulated with PSCs for 12 h (PSC1_12h–PSC3_12h) and 24 h (PSC1_24h–PSC3_24h) and six corresponding control samples (PBS1_12h–PBS3_12h and PBS1_24h–PBS3_24h). In the PSC_12h vs. PBS_12h and PSC_24h vs. PBS_24h groups, 3,520 (2,359 upregulated and 1,161 downregulated) and 3,287 (1765 upregulated and 1,522 downregulated) DEgenes were identified, respectively. The expression of 45 PRRs genes was upregulated in the PSC_12h and PSC_24h groups compared to those in the control groups, including 4 Toll-like receptors (TLRs), 4C-type lectin receptors (CLRs), 3 NOD-like receptors (NLRs), 17 G protein-coupled receptors (GPCRs), 4 scavenger receptors (SRs), and 13 leucine-rich repeat-containing proteins (LRRCs). GO enrichment and KEGG analyses revealed that these DEgenes were mainly involved in the regulation of host immune response processes and molecules. These included antigen processing and presentation, Th17, PI3K-Akt, Th1, and Th2 cell differentiation, neutrophil extracellular trap formation, NOD- and Toll-like receptors, TNF, intestinal immune network for IgA production and IL-17 signaling pathway. Furthermore, the identified DEgenes were involved in the regulation of signaling molecules and interaction (e.g., cell adhesion molecules and ECM-receptor interaction).ConclusionThese preliminary findings provide novel perspectives on the host innate immune response to E. granulosus PSC stimulation, with a focus on the involvement of E. granulosus-specific PRRs in host defense mechanisms against infection.

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TLR10: An intriguing Toll-like receptor with many unanswered questions

Cited by 2 publications

References 62 publications

Human and Murine Toll-like Receptor-Driven Disease in Systemic Lupus Erythematosus

Human and Murine Toll-like Receptor-Driven Disease in Systemic Lupus Erythematosus

RNA sequencing reveals dynamic expression of genes related to innate immune responses in canine small intestinal epithelial cells induced by Echinococcus granulosus protoscoleces

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