Updates on immunological mechanistic insights and targeting of the oral lichen planus microenvironment

Deng, Xiaojuan; Wang, Ying; Jiang, Lu; Li, Jing; Chen, Qianming

doi:10.3389/fimmu.2022.1023213

Cited by 28 publications

(22 citation statements)

References 141 publications

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“…promote the pathological progression of OLP. [39][40][41] At present, glucocorticoids, as the first-line anti-inflammatory and immunosuppression drug, were used in clinical OLP treatment. Although glucocorticoids provided an extent of symptomatic relief, they were prone to side effects and drug resistance.…”

Section: Discussionmentioning

confidence: 99%

“…It has been previously reported that numerous monocytes at the basement membrane of OLP tissue differentiated into M1 macrophages, which intensified inflammation in the lesion area by secreting inflammatory cytokines such as IL-1β, TNF-α. [ 39 ] Mast cell degranulation played an extremely critical role in the OLP’s basement membrane disruption. [ 43 ] Substantial experimental data suggested that helper T cells, including Th1, Th2, Treg, and Th17 subsets, were involved in the pathogenic process of OLP.…”

Section: Discussionmentioning

confidence: 99%

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Development of an immune-related diagnostic predictive model for oral lichen planus

Bian,

Yan,

Chen

et al. 2024

Medicine

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Oral lichen planus (OLP) was a chronic inflammatory disease of unknown etiology with a 1.4% chance of progressing to malignancy. However, it has been suggested in several studies that immune system disorders played a dominant role in the onset and progression of OLP. Therefore, this experiment aimed to develop a diagnostic prediction model for OLP based on immunopathogenesis to achieve early diagnosis and treatment and prevent cancer. In this study, 2 publicly available OLP datasets from the gene expression omnibus database were filtered. In the experimental group (GSE52130), the level of immune cell infiltration was assessed using MCPcounter and ssGSEA algorithms. Subsequently, differential expression analysis and gene set enrichment analysis were performed between the OLP and control groups. The resulting differentially expressed genes were intersected with immunologically relevant genes provided on the immunology database and analysis portal database (ImmPort) website to obtain differentially expressed immunologically relevant genes (DEIRGs). Furthermore, the gene ontology and kyoto encyclopedia of genes and genomes analyses were carried out. Finally, protein–protein interaction network and least absolute shrinkage and selection operator regression analyses constructed a model for OLP. Receiver operating characteristic curves for the experimental and validation datasets (GSE38616) were plotted separately to validate the model’s credibility. In addition, real-time quantitative PCR experiment was performed to verify the expression level of the diagnostic genes. Immune cell infiltration analysis revealed a more significant degree of inflammatory infiltration in the OLP group compared to the control group. In addition, the gene set enrichment analysis results were mainly associated with keratinization, antibacterial and immune responses, etc. A total of 774 differentially expressed genes was obtained according to the screening criteria, of which 65 were differentially expressed immunologically relevant genes. Ultimately, an immune-related diagnostic prediction model for OLP, which was composed of 5 hub genes (BST2, RNASEL, PI3, DEFB4A, CX3CL1), was identified. The verification results showed that the model has good diagnostic ability. There was a significant correlation between the 5 hub diagnostic biomarkers and immune infiltrating cells. The development of this model gave a novel insight into the early diagnosis of OLP.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Development of an immune-related diagnostic predictive model for oral lichen planus

Bian,

Yan,

Chen

et al. 2024

Medicine

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“…However, the causes that initiate and/or perpetuate OLP are still not fully understood, and only a small number of risk factors, such as the immune response, genetic background, infectious agents, stress, and drugs, are currently believed to possibly play a role in OLP pathogenesis 5 . The current literature indicates that immune factors may be key to the pathogenesis of OLP 6,7 . In particular, T‐cells have been shown to be crucial in the development of illness 8 .…”

Section: Introductionmentioning

confidence: 99%

“… 5 The current literature indicates that immune factors may be key to the pathogenesis of OLP. 6 , 7 In particular, T‐cells have been shown to be crucial in the development of illness. 8 In addition, in the early stage of disease development, more apoptotic keratinocytes can be found, 9 indicating that keratinocytes may be target cells in the early stage of disease occurrence.…”

Section: Introductionmentioning

confidence: 99%

PA28γ induces dendritic cell maturation and activates T‐cell immune responses in oral lichen planus

Wang,

Zhang,

Deng

et al. 2024

MedComm

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Oral lichen planus (OLP) is a common chronic inflammatory disease of the oral mucosa, the mechanism of its inflammatory progression has not yet been fully elucidated. PA28γ plays a significant role in a variety of immune‐related diseases. However, the exact role of PA28γ in the pathogenesis of OLP remains unclear. Here, we demonstrated that PA28γ is overexpressed in epithelial cells and inflammatory cells of OLP tissues but has no significant relationship with OLP subtypes. Functionally, keratinocytes with high PA28γ expression could induce dendritic cell (DC) maturation and promote the T‐cell differentiation into Th1 cells in response to the immune response. In addition, we found that a high level of PA28γ expression is associated with high numbers of infiltrating mature DCs and activated T‐cells in OLP tissues. Mechanistically, keratinocytes with high PA28γ expression could promote the secretion of C–C motif chemokine (CCL)5, blocking CCL5 or/and its receptor CD44 could inhibit the induction of T‐cell differentiation by keratinocytes with high PA28γ expression. In conclusion, we reveal that keratinocytes with high expression of PA28γ in OLP can induce DC maturation and promote T‐cell differentiation through the CCL5‐CD44 pathway, providing previously unidentified mechanistic insights into the mechanism of inflammatory progression in OLP.

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“…Lichen planus is a common chronic inflammatory mucosal and skin disorder that affects approximately 0.5–4% of the worldwide population, with a malignant transformation rate of 1.4% [ 1 , 2 ]. Also, OLP had a higher prevalence among middle-aged females [ 3 , 4 ], while it is also rare in children (0.03%) [ 5 ].…”

Section: Introductionmentioning

confidence: 99%

Evaluation of the association between TNF-α-1031 T/C polymorphism with oral lichen planus disease

Marabi,

Mozaffari,

Ghasemi

et al. 2024

BMC Oral Health

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Background Oral lichen planus (OLP) is a T-cell-mediated autoimmune disease that affects the epithelial cells of the oral cavity. This study was performed to investigate any possible relationship between − 1031(T/C) polymorphism (rs1799964) of the tumor necrosis factor α (TNF-α) gene with the risk and severity of oral lichen planus (OLP) disease among an Iranian population. Method Saliva samples were collected from 100 patients with OLP and a similar number of healthy controls (age and sex-matched). Then, DNA was extracted from the collected samples for genotyping TNF-α-1031 T/C polymorphism using the PCR-CTPP method. The results were assessed using SPSS software. Results The findings revealed a significantly higher prevalence of the C allele in OLP patients (53%) compared to healthy controls (36%), suggesting an association between TNF-alpha gene polymorphism and OLP. A multivariate logistic regression analysis supported this finding, as the presence of the C allele was significantly associated with an increased risk of OLP [χ2 = 4.17, p = 0.04, 95% CI = 1.01–2.65, OR = 1.64]. However, our data indicated no significant association between TNF-alpha-1031 T/C gene polymorphism and OLP severity. Conclusions These findings provide the first evidence supporting a possible role of TNF-α-1031 T/C gene polymorphism in OLP susceptibility in the Iranian population. The findings of this study demonstrate a positive association between TNF-α-1031 C/T allele distribution and the risk of OLP disease in the Iranian population. Therefore, carrying the C allele may increase the susceptibility to OLP disease.

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Updates on immunological mechanistic insights and targeting of the oral lichen planus microenvironment

Cited by 28 publications

References 141 publications

Development of an immune-related diagnostic predictive model for oral lichen planus

Development of an immune-related diagnostic predictive model for oral lichen planus

PA28γ induces dendritic cell maturation and activates T‐cell immune responses in oral lichen planus

Evaluation of the association between TNF-α-1031 T/C polymorphism with oral lichen planus disease

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