ScRNA of lichen planus
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE280584 | GEO | 2024/12/14
REPOSITORIES: GEO
Similar Datasets
Project description:An early and sustained clinical response was seen, with 83.3% of patients responsive at week 16. Our molecular data identified a unique, oligoclonal IFN-γ, CD8+, CXCL13+ cytotoxic T-cell population in LP skin and demonstrated a rapid decrease in IFN signature within 2 weeks of treatment, most prominently in the basal layer of the epidermis.
2024-12-14 | GSE280583 | GEO
Project description:Lichen planus (LP) is a chronic, debilitating, inflammatory disease of the skin and mucous membranes that affects 1-2% of Americans. Its molecular pathogenesis remains poorly understood, and there are no FDA-approved treatments. We performed single cell RNA sequencing on blood and affected and unaffected skin from 7 LP patients. LP affected skin exhibited a robust immune infiltrate primarily composed of CD8 T-cells. These cells were specifically recruited by cytokines secreted by both superficial and dermal layers of skin. Basal keratinocytes and fibroblasts secrete CXCL9 and CXCL10, and fibroblasts secrete CCL19. Molecular analysis of LP skin and blood samples increased our understanding of disease pathogenesis and identified CCL19 as a new therapeutic target for treatment.
2024-10-03 | GSE254542 | GEO
Project description:Ruxolitinib is a Janus kinase 1/2 inhibitor (JAK1/2) that blocks signal transduction of interferon-gamma, a critical cytokine involved in the pathogenesis of cutaneous lichen planus (LP). In this prospective phase II study, we investigated the efficacy of topical ruxolitinib in cutaneous LP and performed transcriptomic analysis pre- and post-therapy. Twelve patients with cutaneous LP applied topical ruxolitinib twice daily for 8 weeks. Primary endpoints were change in total lesion count and modified Composite Assessment of Index Lesion Severity (mCAILS) score in index treated and untreated index control lesions at week 4. Total lesion count decreased by a median of 50 lesions (interquartile range 25, 723; p<0.001). mCAILS scores decreased by a mean difference of 7.6 (standard deviation 8.8, p=0.016) between index treated and control lesions. Type I and II interferon pathways were enriched in LP and responsive disease displayed downregulation of interferon-stimulated genes (ISGs). In this small pilot study, topical ruxolitinib was highly effective in the treatment of cutaneous LP. Transcriptomic analysis confirmed LP as an interferon-driven disease and downregulation of ISGs correlated with disease response.
2022-01-13 | GSE193351 | GEO
Project description:Lichen planus (LP) is a T cell-mediated disease affecting the stratified squamous epithelia of the skin and/or mucus membrane. Histologically, the disease is characterized by a lichenoid inflammatory infiltrate and vacuolar degeneration of the basal layer of the epidermis. LP has three major subtypes: Cutaneous, mucosal and appendageal LP. Rarely, it may affect the nails in the absence of skin and/or mucosal changes. LP may also be induced by several drugs, typically anti-hypertensive medication or be associated with infections, particularly viral hepatitis. The diagnosis is based on the clinical presentation and characteristic histological findings. Although the disease is often self-limiting, the intractable pruritus and painful mucosal erosions result in significant morbidity. The current first-line treatment are topical and/or systemic corticosteroids. In addition, immunosuppressants may be used as corticosteroid-sparing agents. These, however are often not sufficient to control disease. Janus kinase inhibitors and biologics (anti-IL-12/23, anti-IL17) have emerged as novel future treatment options. Thus, one may expect a dramatic change of the treatment landscape of LP in the near future.
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Project description:Lichen planus (LP) is a dermatosis without a fully understood etiopathogenesis, the frequency of which is estimated to be less than 1% among the population. LP may involve the glabrous skin, mucosal membranes, scalp, nails and genital area. Nowadays, there are reports of its association with lipid homeostasis aberrations. In this review, we present the contemporary view of this matter. Dyslipidemia, especially hypertriglyceridemia, seems to be an actual problem in this group of patients, and along with abnormal arterial vessel parameters, indicates an increased risk of atherosclerosis in these subjects. Dermatologists should be attentive to this relationship and aware that the patients may develop different metabolic complications. More studies are required to establish clear guidelines on the management of lipid aberrations in lichen planus.
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Project description:Oral lichen planus (OLP) is a common chronic inflammatory disease of the oral mucosa. The prevalence rate of OLP in adults is 0.5%-2%. The etiology and pathogenesis of OLP are still unclear. The pathogenesis of OLP may be related to the genetic polymorphism of some genes. Currently, the gene families, including tumor necrosis factor, interferon, interleukin, enzyme, and receptor, have been extensively studied. This work reviews related studies on gene polymorphism of OLP.
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Project description:Lichen planus is a chronic disease affecting the skin, appendages, and mucous membranes. A cutaneous lichen planus is a rare disease occurring in less than 1% of the general population, while oral illness is up to five times more prevalent; still, both forms equally impair the patient's quality of life. The etiology of lichen planus is not entirely understood. Yet, immune-mediated mechanisms have been recognized since environmental factors such as hepatitis virus infection, mechanical trauma, psychological stress, or microbiome changes can trigger the disease in genetically susceptible individuals. According to current understanding, lichen planus immunopathogenesis is caused by cell-mediated cytotoxicity, particularly cytotoxic T lymphocytes, whose activity is further influenced by Th1 and IL-23/Th-17 axis. However, other immunocytes and inflammatory pathways complement these mechanisms. This paper presents a comprehensive insight into the actual knowledge about lichen planus, with the causal genetic and environmental factors being discussed, the immunopathogenesis described, and the principal effectors of its inflammatory circuits identified.
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Project description:Vulvar lichen planus (VLP) is a chronic inflammatory disease which adversely affects patients' quality of life. The pathogenesis of VLP is unknown although Th1 immune response has been implicated. We aimed to discover specific tissue-based protein biomarkers in VLP compared to normal vulvar tissue (NVT), vulvar lichen sclerosus (VLS) and oral lichen planus (OLP). We used laser capture microdissection-liquid chromatography- tandem mass spectrometry to assess protein expression in fixed lesional mucosal specimens from patients with VLP (n = 5). We then compared proteomic profiles against those of NVT (n = 4), VLS (n = 5), OLP (n = 6) and normal oral mucosa (n = 5), previously published by our group. IL16, PTPRC, PTPRCAP, TAP1 and ITGB2 and were significantly overexpressed in VLP compared to NVT. Ingenuity pathway analysis identified antigen presentation and integrin signalling pathways. Proteins overexpressed in both VLP versus NVT and OLP versus NOM included IL16, PTPRC, PTPRCAP, TAP1, HLA-DPB1, HLA-B and HLA-DRA. This proteomic analysis revealed several overexpressed proteins in VLP that relate to Th1 autoimmunity, including IL16. Overlapping pathways, including those involving IFNγ and Th1 signalling, were observed between VLP, VLS, and OLP.
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Project description:Oral lichen planus is a chronic inflammatory disease of established immune-mediated pathogenesis that affects the oral mucosa. Polycythemia is a nonaggressive myeloproliferative disorder, characterized by an increase in red blood cell mass, often with uncontrolled production of granulocytes and platelets. Their association was rarely mentioned in the scientific literature. The aim of this paper was to report their occurrence in a 52-year-old male patient. Although a casual connection cannot be excluded, both diseases share many similarities in the immune dysfunctions involved in their pathogenesis and their clinical features. Such a hypothesis remains to be demonstrated by further studies. The presence of oral lesions should alert the clinicians in the process of identifying and early diagnosing these diseases. Thus, complications can be prevented and treatment can be started at an early stage, avoiding further damage.
| S-EPMC7428844 | biostudies-literature
Project description:Oral lichen planus (OLP) is a chronic disease of uncertain etiology, although it is generally considered as an immune-mediated disease that affects the mucous membranes and even the skin and nails. Over the years, this disease was attributed to a variety of causes, including different types of microorganisms. This review analyzes the present state of the art of the disease, from a microbiological point of view, while considering whether or not the possibility of a microbial origin for the disease can be supported. From the evidence presented here, OLP should be considered an immunological disease, as it was initially proposed, as opposed to an illness of microbiological origin. The different microorganisms so far described as putative disease-causing agents do not fulfill Koch’s postulates; they are, actually, not the cause, but a result of the disease that provides the right circumstances for microbial colonization. This means that, at this stage, and unless new data becomes available, no microorganism can be envisaged as the causative agent of lichen planus.
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