TLR10: Insights, controversies and potential utility as a therapeutic target

Su, Si-Biao; Lin, Tao; Deng, Ze-Ping; Chen, Wen; Qin, Shanyu; Jiang, Haixing

doi:10.1111/sji.12988

Cited by 39 publications

(30 citation statements)

References 96 publications

(283 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…By contrast, TLR3, TLR7, TLR8, and TLR9 localize to endosomes, where they detect nucleic acids derived from viruses, bacteria, or damaged cells. The roles of TLR10 and TLR11 remain unclear, and TLR10 seems to be able to form dimers with TLR1-2, TLR4, TLR6, and TLR8 [ 84 , 85 , 86 , 87 ]. Once the PRRs on the surface of the target cell have been activated by PAMPs or DAMPs, they initiate the innate immune response by producing chemokines, cytokines, and antimicrobial peptides (AMPs).…”

Section: C Acnes and Inflammationmentioning

confidence: 99%

Cutibacterium acnes as an Opportunistic Pathogen: An Update of Its Virulence-Associated Factors

2021

View full text Add to dashboard Cite

Cutibacterium acnes is a member of the skin microbiota found predominantly in regions rich in sebaceous glands. It is involved in maintaining healthy skin and has long been considered a commensal bacterium. Its involvement in various infections has led to its emergence as an opportunist pathogen. Interactions between C. acnes and the human host, including the human skin microbiota, promote the selection of C. acnes strains capable of producing several virulence factors that increase inflammatory capability. This pathogenic property may be related to many infectious mechanisms, such as an ability to form biofilms and the expression of putative virulence factors capable of triggering host immune responses or enabling C. acnes to adapt to its environment. During the past decade, many studies have identified and characterized several putative virulence factors potentially involved in the pathogenicity of this bacterium. These virulence factors are involved in bacterial attachment to target cells, polysaccharide-based biofilm synthesis, molecular structures mediating inflammation, and the enzymatic degradation of host tissues. C. acnes, like other skin-associated bacteria, can colonize various ecological niches other than skin. It produces several proteins or glycoproteins that could be considered to be active virulence factors, enabling the bacterium to adapt to the lipophilic environment of the pilosebaceous unit of the skin, but also to the various organs it colonizes. In this review, we summarize current knowledge concerning characterized C. acnes virulence factors and their possible implication in the pathogenicity of C. acnes.

show abstract

Section: C Acnes and Inflammationmentioning

confidence: 99%

Cutibacterium acnes as an Opportunistic Pathogen: An Update of Its Virulence-Associated Factors

2021

View full text Add to dashboard Cite

show abstract

“…Furthermore, TLR10 may heterodimerize with TLR2 to recognize LPS and heat shock proteins (HSP60) of Helicobacter pylori ( H. pylori ) to trigger innate immune responses. PamCysPamSK4, a diacylated peptide, could be recognized by the TLR10 homodimer and TLR1/TLR10 heterodimer (Fore et al 2020 ; Su et al 2020 ). A recent study has shown that TLR10 can enhance gp41-mediated IL-8 induction and NF-κBα activation and modulate HIV-1 infection and integration independent of TLR2 (Henrick et al 2019 ).…”

Section: Lipoprotein Is the Predominant Ligand For The Tlr2 Subfamilymentioning

confidence: 99%

“…Moreover, TLR10 can upregulate chemokine ligand 20 and IL-8 expression in response to Listeria monocytogenes (EGD) and Salmonella typhimurium ( S. typhimurium ) infections, while the infection with H1N1 (A/HK/54/98) and H5N1 (A/Vietnam/3212/04) influenza virus leads to an increased TLR10 expression and triggers the induction of pro-inflammatory cytokines and interferons in the host (Latorre et al 2016 ; Lee et al 2014a , 2014b ; Regan et al 2013 ). TLR10 is the only TLR that can antagonize TLR2 activity, inhibit downstream signal transductions, and suppress B cell adaptive immune responses (Hess et al 2017 ; Oosting et al 2014 ; Su et al 2020 ). It acts as a negative regulator of both MyD88 and TRIF-mediated signaling, suppressing the degradation of IκB and the phosphorylation of MAPKs through the production of IFN-β (Jiang et al 2016 ).…”

Section: Lipoprotein Is the Predominant Ligand For The Tlr2 Subfamilymentioning

confidence: 99%

Research progress on Toll-like receptor signal transduction and its roles in antimicrobial immune responses

Xia

Lian

et al. 2021

Appl Microbiol Biotechnol

View full text Add to dashboard Cite

When microorganisms invade a host, the innate immune system first recognizes the pathogen-associated molecular patterns of these microorganisms through pattern recognition receptors (PRRs). Toll-like receptors (TLRs) are known transmembrane PRRs existing in both invertebrates and vertebrates. Upon ligand recognition, TLRs initiate a cascade of signaling events; promote the pro-inflammatory cytokine, type I interferon, and chemokine expression; and play an essential role in the modulation of the host’s innate and adaptive immunity. Therefore, it is of great significance to improve our understanding of antimicrobial immune responses by studying the role of TLRs and their signal molecules in the host’s defense against invading microbes. This paper aims to summarize the specificity of TLRs in recognition of conserved microbial components, such as lipoprotein, lipopolysaccharide, flagella, endosomal nucleic acids, and other bioactive metabolites derived from microbes. This set of interactions helps to elucidate the immunomodulatory effect of TLRs and the signal transduction changes involved in the infectious process and provide a novel therapeutic strategy to combat microbial infections.

show abstract

“…Furthermore, depending on the type of dimer formed, TLR10 is suggested to be able to produce a pro-inflammatory or an inhibitory effect. 100 Similarly, mixed results have emerged for the role of TLR10 in RA. In line with TLR10 having an anti-inflammatory role, TLR10 mRNA is expressed at lower levels in PBMCs of RA patients with active disease, whilst a missense mutation (I473T) has been associated with increased disease severity and a lower response to the anti-TNF biological infliximab.…”

Section: Tlr10mentioning

confidence: 99%

Contribution of Toll-Like Receptors and the NLRP3 Inflammasome in Rheumatoid Arthritis Pathophysiology

Unterberger¹,

Davies²,

Rambhatla³

et al. 2021

ITT

View full text Add to dashboard Cite

Rheumatoid arthritis (RA) is a progressive autoimmune disease that is characterized by inflammation of the synovial joints leading to cartilage and bone damage. The pathogenesis is sustained by the production of pro-inflammatory cytokines including tumor necrosis factor (TNF), interleukin (IL)-1 and IL-6, which can be targeted therapeutically to alleviate disease severity. Several innate immune receptors are suggested to contribute to the chronic inflammation in RA, through the production of pro-inflammatory factors in response to endogenous danger signals. Much research has focused on toll-like receptors and more recently the nucleotide-binding domain and leucine-rich repeat pyrin containing protein-3 (NLRP3) inflammasome, which is required for the processing and release of IL-1β. This review summarizes the current understanding of the potential involvement of these receptors in the initiation and maintenance of inflammation and tissue damage in RA and experimental arthritis models.

show abstract

TLR10: Insights, controversies and potential utility as a therapeutic target

Cited by 39 publications

References 96 publications

Cutibacterium acnes as an Opportunistic Pathogen: An Update of Its Virulence-Associated Factors

Cutibacterium acnes as an Opportunistic Pathogen: An Update of Its Virulence-Associated Factors

Research progress on Toll-like receptor signal transduction and its roles in antimicrobial immune responses

Contribution of Toll-Like Receptors and the NLRP3 Inflammasome in Rheumatoid Arthritis Pathophysiology

Contact Info

Product

Resources

About