ArticleJournal of inflammation (London, England)2014
Role of toll-like receptors in human iris pigment epithelial cells and their response to pathogen-associated molecular patterns.
Article in Journal of inflammation (London, England), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.
- Ocular Microbiota and Intraocular Inflammation.Frontiers in immunology · 2020Pooled it
- Article
- The curious case of AAV immunology.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- The contribution of pattern recognition receptor signalling in the development of age related macular degeneration: the role of toll-like-receptors and the NLRP3-inflammasome.Journal of neuroinflammation · 2024Review
- Morroniside ameliorates lipopolysaccharide-induced inflammatory damage in iris pigment epithelial cells through inhibition of TLR4/JAK2/STAT3 pathway.International journal of ophthalmology · 2023Article
- Pathogenesis and Manifestations of Zika Virus-Associated Ocular Diseases.Tropical medicine and infectious disease · 2022Review
- An analysis of the clinical profile of patients with uveitis following COVID-19 infection.Indian journal of ophthalmology · 2022Observational
- Low-dose melittin is safe for intravitreal administration and ameliorates inflammation in an experimental model of uveitis.Current research in pharmacology and drug discovery · 2022Article
- The Cellular Composition of the Uveal Immune Environment.Frontiers in medicine · 2021Review
- Zika Virus Infection of Human Iris Pigment Epithelial Cells.Frontiers in immunology · 2021Article
- Intraocular Biopsy and ImmunoMolecular Pathology for "Unmasking" Intraocular Inflammatory Diseases.Journal of clinical medicine · 2019Review
- Article
- Associations of TLR4 gene polymorphisms with the risk of age-related macular degeneration in a Chinese Han population.Medicine · 2019Article
- Effect of berberine on lipopolysaccharide-induced monocyte chemotactic protein-1 and interleukin-8 expression in a human retinal pigment epithelial cell line.International ophthalmology · 2018Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundToll-like receptor (TLR) activation is hypothesized to contribute to inflammatory eye disease including uveitis, yet the distribution pattern of TLRs in human uveal tissues remains poorly described. The purpose of this study was to investigate the expression profile of TLRs in human iris pigment epithelial cells (IPE) at the gene and protein level and examine the effect of pathogen-associated molecular patterns (PAMPs), such as Pam3CSK4.3HCl, Poly(I:C), lipopolysaccharides (LPS from E. coli serotype O111:B4), Flagellin, MALP-2 (macrophage activating lipopeptide-2), Poly(U) and CpGODN2395 on the production of inflammatory mediators including interleukin-8 (IL-8) and monocyte chemotactic protein 1 (MCP-1) from human IPE and retinal pigment epithelial cells (RPE).
methodsRT-PCR and Western blotting was employed to investigate the expression of TLRs 1-10 in primary IPE and RPE. Secretion of IL-8 or MCP-1 following treatment with PAMPs was measured by ELISA. The role of TLR2, TLR3 and TLR4 in mediating an inflammatory response was investigated using pharmacological TLR inhibitors.
resultsIPE and RPE expressed transcripts for TLR1-6 and 8-10; and proteins for TLR1-6 and 9. IPE secreted IL-8 or MCP-1 in response to Pam3CSK4.3HCl, Poly(I:C), LPS and MALP-2, whereas RPE produced IL-8 only after Poly(I:C), LPS or MALP-2 treatment. TLR inhibitors (OxPAPC, CI-095 and chloroquine) blocked IL-8 secretion in Poly(I:C), LPS or MALP-2-treated IPE and RPE.
conclusionsOcular pigment epithelial cells respond to PAMPs through activation of TLRs, particularly TLR2, TLR3 and TLR4. Expression of TLRs in human IPE cells provides a basis for responses to many ocular pathogens and their activation may be involved in the pathogenesis of ocular inflammation.
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