Increased gene expression of Toll‐like receptor 4 on peripheral blood mononuclear cells in patients with psoriasis

García‐Rodríguez, Sonia; Arias‐Santiago, Salvador; Perandrés-López, Rubén; Castellote, Laura; Zumaquero, Esther; Navarro, Pilar; Buendía‐Eisman, A.; Ruiz, J.C.; Orgaz‐Molina, Jacinto; Sancho, Jaime; Zubiaur, Mercedes

doi:10.1111/j.1468-3083.2011.04372.x

Cited by 65 publications

(48 citation statements)

References 56 publications

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“…The results support the involvement of innate immune response elements in the pathophysiology of psoriasis, in line with previous studies (12,17,(22)(23)(24)26,27,(32)(33)(34)(35)(36), although some previous studies have reported conflicting results regarding TLR-9 expression in psoriasis (22,34). The activation of IL-33, TLR-2 and TLR-9 in psoriatic plaques may be important since such activation has been previously associated with the activation of NF-κB (12,23,37).…”

Section: Discussionsupporting

confidence: 80%

Effect of TNF-α inhibitors on transcriptional levels of pro-inflammatory interleukin-33 and Toll-like receptors-2 and -9 in psoriatic plaques

Vageli

Exarchou

Zafiriou

et al. 2015

Experimental and Therapeutic Medicine

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Abstract. Tumor necrosis factor (TNF)-α inhibitors are considered to be effective in the treatment of psoriatic plaques, although the precise therapeutic pathway is not clear. Pro-inflammatory molecules, such as Toll-like receptor (TLR)-2 and -9 and interleukin (IL)-33, a member of the IL-1 receptor/TLR superfamily, have been found to be expressed in psoriatic plaques. The aim of the present study was to investigate whether TNF-α inhibitor treatment has an effect on the expression of IL-33 and TLR-2 and -9 in psoriatic plaques. Seventeen patients with psoriatic plaques were treated with a TNF-α inhibitor (etanercept or infliximab) for 12 weeks in an open-label study, and the transcriptional levels of IL-33 and TLR-2 and -9 were determined by reverse transcription-quantitative polymerase chain reaction in paired biopsies of psoriatic plaques obtained at baseline (B) and following the 12 weeks of treatment (P). The psoriasis area severity index (PASI) score was also determined. At B, elevated IL-33 and TLR-2 mRNA levels were observed in all cases, while TLR-9 showed elevated mRNA levels in 76% of cases. At P, reductions in the mRNA levels of IL-33, TLR-2 and TLR-9 were observed, with TLR-2 and -9 levels exhibiting significant reductions (P<0.0001, Wilcoxon signed-rank test). PASI scores were significantly reduced by the treatment (P<0.0001, Wilcoxon signed-rank test) and the changes in PASI scores exhibited a significant positive Pearson's correlation with the P/B mRNA expression ratios of TLR-2 or -9 in males (P<0.05), particularly in the etanercept group (P<0.0001). The findings support the efficacy of anti-TNF-α treatment on the innate immune response in psoriatic skin, with a focus on TLR-2 and -9 inhibition, suggesting their role in the pathogenic mechanism of plaque psoriasis, which may be associated with gender.

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Section: Discussionsupporting

confidence: 80%

Effect of TNF-α inhibitors on transcriptional levels of pro-inflammatory interleukin-33 and Toll-like receptors-2 and -9 in psoriatic plaques

Vageli

Exarchou

Zafiriou

et al. 2015

Experimental and Therapeutic Medicine

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“…On the other hand, Toll‐like receptors (TLRs) of epidermal cells are transmembrane proteins, with the extracellular portions or the intracellular portions conjugated to corresponding ligands, capable of initiating innate immune responses and influencing subsequent adaptive immune responses 31, 32. Evidence supported that TLR4 in immune response has been revealed in the pathogenesis of psoriasis 33, and increased gene expression of TLR4 on peripheral blood mononuclear cells in patients with psoriasis was revealed 34. In addition, although the negative correlation of TLR4 with miR181‐b has been revealed in a previous study in acute myeloid leukaemia 35, whether such a correlation was still existed in on psoriasis pathogenesis remains unexplored.…”

Section: Introductionmentioning

confidence: 99%

Retracted: MicroRNA‐181b negatively regulates the proliferation of human epidermal keratinocytes in psoriasis through targeting TLR4

Feng

Bai

et al. 2016

J Cellular Molecular Medi

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Our study aims to explore the role of microRNA‐181b (miR‐181b) and TLR in the regulation of cell proliferation of human epidermal keratinocytes (HEKs) in psoriasis. Twenty‐eight patients diagnosed with psoriasis vulgaris were selected as a case group with their lesional and non‐lesional skin tissues collected. A control group consisted of 20 patients who underwent plastic surgery with their healthy skin tissues collected. Real‐time quantitative fluorescence polymerase chain reaction (RT‐qPCR), in situ hybridization and immunohistochemistry were used to detect the expressions of miR‐181b and TLR4 in HEKs of healthy skin, psoriatic lesional skin and non‐lesional skin respectively. The 3′ untranslated region (3′UTR) of TLR4 combined with miR‐181b was verified by a dual‐luciferase reporter assay. Western blotting and bromodeoxyuridine were applied for corresponding detection of TLR4 expression and cell mitosis. The expression of miR‐181b in HEKs of psoriatic lesional skin was less than healthy skin and psoriatic non‐lesional skin. In psoriatic lesional and non‐lesional skin, TLR4‐positive cell rates and the number of positive cells per square millimetre were higher than healthy skin. The dual‐luciferase reporter assay verified that miR‐181b targets TLR4. HEKs transfected with miR‐181b mimics had decreased expression of TLR4, along with the decrease of mitotic indexes and Brdu labelling indexes. However, HEKs transfected with miR‐181b inhibitors showed increased TLR4 expression, mitotic indexes and Brdu labelling indexes. HEKs transfected with both miR‐181b inhibitors and siTLR4 had decreased mitotic indexes and Brdu labelling indexes. These results indicate that miR‐181b can negatively regulate the proliferation of HEKs in psoriasis by targeting TLR4.

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“…These mice had exaggerated inflammatory response when challenged by exogenous stimuli such as abrasion (Koebner phenomenon), potentiated inflammation by acting directly as a chemoattractant for leukocytes [13]. Differential Toll-like receptor (TLR4/2) genes expression on psoriatic peripheral blood mononuclear cells were correlated with regulatory proinflammatory cytokines and damage-associated molecule (S100A9) that emphasize innate immune response role in psoriasis [14].…”

Section: Discussionmentioning

confidence: 97%

Psoriasin: A Novel Marker Linked Obesity with Psoriasis

et al. 2013

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Abstract.To evaluate the role of psoriasin, koebnerisin, interleukn (IL)-12 and IL-23 in the pathogenesis of psoriasis and their relations to Psoriasis Area Severity Index (PASI) and obesity. Thirty patients had chronic plaque psoriasis and 30 healthy subjects matched in age and sex were enrolled in this study. Serum from all subjects were used for determination of psoriasin, koebnerisin, IL-12 and IL-23 by ELISA kits. IL-23 and psoriasin were significantly higher in skin psoriasis compared to controls and psoriatic arthritis (PsA). There was a correlation between psoriasin and both PASI and obesity. On the other hand, IL-12 was significantly increased in PsA compared to skin psoriasis (p = 0.000) and controls. Its sensitivity and specificity were 87%, 93%; respectively. To our knowledge, psoriasin is the first biomarker confirm the link between obesity and psoriasis. The risk of developing psoriasis is directly related to higher BMI.

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Increased gene expression of Toll‐like receptor 4 on peripheral blood mononuclear cells in patients with psoriasis

Abstract: Differential TLR4 ⁄ 2 gene expressions on psoriatic peripheral blood mononuclear cells and correlations with regulatory and ⁄ or proinflammatory cytokines and ⁄ or damage-associated molecular pattern molecule S100A9 emphasize innate immune response role in psoriasis.

Cited by 65 publications

References 56 publications

Effect of TNF-α inhibitors on transcriptional levels of pro-inflammatory interleukin-33 and Toll-like receptors-2 and -9 in psoriatic plaques

Effect of TNF-α inhibitors on transcriptional levels of pro-inflammatory interleukin-33 and Toll-like receptors-2 and -9 in psoriatic plaques

Retracted: MicroRNA‐181b negatively regulates the proliferation of human epidermal keratinocytes in psoriasis through targeting TLR4

Psoriasin: A Novel Marker Linked Obesity with Psoriasis

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