Distinct interferon‐gamma and interleukin‐9 expression in cutaneous and oral lichen planus

Weber, Benedikt; Schlapbach, Christoph; Stuck, M.; Simon, Hans‐Uwe; Borradori, Luca; Beltraminelli, Helmut; Simon, Dagmar

doi:10.1111/jdv.13989

Cited by 29 publications

(31 citation statements)

References 53 publications

(123 reference statements)

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“…However, the etiology and pathogenesis of OLP are not well understood. Acanthosis is the frequent pathological change in OLP tissues . Besides the two features of OLP, a dense sub‐epithelium of mainly T lymphocytic infiltration and vacuolar degeneration of the basal layer, keratinocyte apoptosis is often found within or beneath the epidermis of OLP .…”

Section: Introductionmentioning

confidence: 99%

Down‐regulation of miRNA‐27b‐3p suppresses keratinocytes apoptosis in oral lichen planus

Chen

Wang

et al. 2019

J Cellular Molecular Medi

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Oral lichen planus (OLP) is considered a precancerous lesion with no known cure. Recent studies reported that abnormal regulation of apoptosis was involved in the pathogenesis of OLP. Next generation sequencing was used to screen the candidate microRNAs and genes in biopsies from patients with OLP and healthy mucosa. Human oral keratinocytes were transfected into the related oligonucleotides of miR‐27b‐3p/cyclophilin D and their control groups. Apoptosis was detected by TdT‐mediated dUTP nick end labelling and flow cytometry. The levels of mRNA and protein were detected by quantitative PCR, Western blots, and enzyme‐linked immunosorbent assays, respectively. Luciferase assays were performed to detect the luciferase activities of miR‐27b‐3p and cyclophilin D. Here, we showed that basal epithelium apoptosis was reduced and the miR‐27b‐3p levels were decreased in clinical OLP samples. We also found that down‐regulation of miR‐27b‐3p inhibited epithelial keratinocyte apoptosis by up‐regulating cyclophilin D expression. Moreover, cyclophilin D increased the protein stability of Bcl2 through direct binding, and Bcl2 suppressed caspase9/3 activation and cytochrome C release. Taken together, these data showed that miR‐27b‐3p regulated keratinocyte apoptosis through cyclophilin D/Bcl2 signalling, suggesting the miR‐27b‐3p regulated the pathogenesis of OLP.

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Section: Introductionmentioning

confidence: 99%

Down‐regulation of miRNA‐27b‐3p suppresses keratinocytes apoptosis in oral lichen planus

Chen

Wang

et al. 2019

J Cellular Molecular Medi

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“…Although the exact causes of this lichenoid tattoo reaction are not yet identified, based on previous reports, we suggest that this reaction might be due to an autoimmune disease . The mechanism of this tattoo‐stimulated lichenoid reaction can be explained.…”

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confidence: 67%

Oral bullous lichenoid tattoo reaction against red dyes on the lips

Zeng

Xiang

2019

Int J Dermatology

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“…Observational studies described high numbers of cytotoxic T cells in LE and LP lesions (de Carvalho et al, 2016;Wenzel and Tuting, 2008). A dominance of type I immune cells could be detected by transcriptome analysis of LE skin lesions (Jabbari et al, 2014), and a high IFN-g expression was measured in oral and cutaneous LP (Weber et al, 2017). NFkB IRF2 IRF1 RELA STAT1 AP-1 IFIH1 CCL8 CFB RSAD2 CXCL10 ISG20 MX2 IFIT2 CIITA IL15 HLA-DRB1 CSF3 CD74 CD83 HLA-DMA TLR2 HLA-DRA TNFAIP2 OAS1 ELF3 CD38 BIRC3 CCL3 CCL5 HLA-DMB CXCL2 CCL2 AIM2 C3 TNFAIP3 CTSS IL7R GBP1 IFITM1 TNFSF13B CXCL9 IL18BP PSMB9 TAP1 ICAM1 IL1B MMP9 CSF2 TNF CXCL11 IFN-γ + TNF-α Furthermore, genetic polymorphisms of IFN-g are linked to LP susceptibility (Al-Mohaya et al, 2016).…”

Section: Discussionmentioning

confidence: 95%

Type I Immune Response Induces Keratinocyte Necroptosis and Is Associated with Interface Dermatitis

Lauffer

Jargosch

Krause

et al. 2018

Journal of Investigative Dermatology

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Interface dermatitis is a characteristic histological pattern that occurs in autoimmune and chronic inflammatory skin diseases. It is unknown whether a common mechanism orchestrates this distinct type of skin inflammation. Here we investigated the overlap of two different interface dermatitis positive skin diseases, lichen planus and lupus erythematosus. The shared transcriptome signature pointed toward a strong type I immune response, and biopsy-derived T cells were dominated by IFN-γ and tumor necrosis factor alpha (TNF-α) positive cells. The transcriptome of keratinocytes stimulated with IFN-γ and TNF-α correlated significantly with the shared gene regulations of lichen planus and lupus erythematosus. IFN-γ, TNF-α, or mixed supernatant of lesional T cells induced signs of keratinocyte cell death in three-dimensional skin equivalents. We detected a significantly enhanced epidermal expression of receptor-interacting-protein-kinase 3, a key regulator of necroptosis, in interface dermatitis. Phosphorylation of receptor-interacting-protein-kinase 3 and mixed lineage kinase domain like pseudokinase was induced in keratinocytes on stimulation with T-cell supernatant-an effect that was dependent on the presence of either IFN-γ or TNF-α in the T-cell supernatant. Small hairpin RNA knockdown of receptor-interacting-protein-kinase 3 prevented cell death of keratinocytes on stimulation with IFN-γ or TNF-α. In conclusion, type I immunity is associated with lichen planus and lupus erythematosus and induces keratinocyte necroptosis. These two mechanisms are potentially involved in interface dermatitis.

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Distinct interferon‐gamma and interleukin‐9 expression in cutaneous and oral lichen planus

Cited by 29 publications

References 53 publications

Down‐regulation of miRNA‐27b‐3p suppresses keratinocytes apoptosis in oral lichen planus

Down‐regulation of miRNA‐27b‐3p suppresses keratinocytes apoptosis in oral lichen planus

Oral bullous lichenoid tattoo reaction against red dyes on the lips

Type I Immune Response Induces Keratinocyte Necroptosis and Is Associated with Interface Dermatitis

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