Myeloid dendritic cells stimulated by thymic stromal lymphopoietin promote Th2 immune responses and the pathogenesis of oral lichen planus

Yamauchi, Masaki; Moriyama, Masafumi; Mitsui, Takashi; Ishiguro, Nozomu; Kubota, Keigo; Furukawa, Soichi; Ohta, Miho; Sakamoto, M.; Tanaka, Akihiko; Nakamura, Seiji

doi:10.1371/journal.pone.0173017

Cited by 28 publications

(24 citation statements)

References 23 publications

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“…However, a recent study has suggested that Th2‐mediated inflammation can also contribute to the pathogenesis of oral lichen planus and that its progression can be induced by myeloid dendritic cells, which in turn are activated by thymic stromal lymphopoietin secreted by epithelial cells. Cytokine polymorphisms seem also to influence whether lesions would only develop in the mouth (interferon gamma‐associated) or also on the skin (tumor necrosis factor alpha‐associated) . A recent meta‐analysis has confirmed the association between −308 G/A polymorphism in tumor necrosis factor alpha gene and oral lichen planus .…”

Section: Oral Lichen Planusmentioning

confidence: 98%

Oral lichen planus: A disease or a spectrum of tissue reactions? Types, causes, diagnostic algorhythms, prognosis, management strategies

Carrozzo

Porter

Mercadante

et al. 2019

Periodontology 2000

150

167

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| INTRODUC TI ONOral lichen planus and lichenoid lesions comprise a group of disorders of the oral mucosa that likely represent a common reaction pattern in response to extrinsic antigens, altered self-antigens or super antigens. 1 Historically, there have been unresolved debates and controversies around the oral lichen planus and lichenoid lesions terminology. The latter term has frequently been used to refer to oral lesions that have clinical and histopathological features similar to oral lichen planus but no risk of malignant transformation, or to indicate an uncertain diagnosis of oral lichen planus. However, definitive clinical and histological diagnostic criteria able to distinguish oral lichen planus from lichenoid lesions are still lacking. 1 Furthermore, there remains no consensus regarding the possible different clinical behavior of the disorders in the oral lichen planus and lichenoid lesions group with respect to cancer development. In dermatology, the concept of 'lichenoid tissue reaction/interface dermatitis' was introduced a long time ago to define a number of distinct inflammatory cutaneous diseases sharing common histopathological features, including liquefactive/vacuolar changes of the basal keratinocytes and a subepithelial band-like array of mononuclear inflammatory cells, including activated T lymphocytes, macrophages, and dendritic cells. 1,2 During the 2006 World Workshop in Oral Medicine IV, it was proposed to classify the oral lichen planus and lichenoid lesions group in 4 distinct disorders, including oral lichen planus, oral lichenoid drug reactions caused by systemic drug exposure, oral lichenoid contact lesions triggered by local hypersensitive reaction to dental materials, and oral lichenoid lesions of graft-vs.-host disease. 3 Although a step forward, this classification failed to provide clear and reliable clinical and histological criteria to properly differentiate these 3 types of lichenoid lesions from oral lichen planus. In addition, several other disease entities characterized by clinical and/or histological features of lichenoid tissue reaction/interface dermatitis were excluded from the classification. Other authors have proposed alternative classifications. 4-6 Overall, there remains no consensus on classification, diagnostic criteria, clinical behavior, and management of the oral lichen planus and lichenoid lesions. 7-9In this review, we have attempted to (i) update the classification of oral lichen planus and lichenoid lesions, (ii) suggest pragmatic diagnostic criteria, and (iii) define a management strategy. Table 1 lists the main disorders displaying histological and/or clinical characteristics of this oral lichen planus and lichenoid lesions group. | CL A SS IFIC ATI ONSome of these disorders are apparently uncommon whereas others are poorly defined or may simply represent a misnomer. | OR AL LI CHEN PL AN USOral lichen planus is the prototype disorder of the group. Despite the lack of reliable epidemiological data, oral lichen planus is thought to be relatively commo...

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Section: Oral Lichen Planusmentioning

confidence: 98%

Oral lichen planus: A disease or a spectrum of tissue reactions? Types, causes, diagnostic algorhythms, prognosis, management strategies

Carrozzo

Porter

Mercadante

et al. 2019

Periodontology 2000

150

167

View full text Add to dashboard Cite

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“…9,10 Previous studies reported overexpression of CCL17 and CCR4 in OLP tissue. 14,15 However, to date, no data are available on the expression levels of CCL17 and CCR4 in the peripheral blood of patients with OLP. In addition, the biological roles of the CCL17-CCR4 axis in OLP remain unexplored.…”

Section: Introductionmentioning

confidence: 99%

Potential roles of the CCL17‐CCR4 axis in immunopathogenesis of oral lichen planus

Shan

Shen

Fang

et al. 2019

J Oral Pathology Medicine

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Background: Oral lichen planus (OLP) is a T cell-mediated chronic inflammatory disease. C-C chemokine receptor type 4 (CCR4) and its cognate C-C motif chemokine ligand 17 (CCL17) play a key role in T-cell activation and trafficking, but their implication in OLP pathogenesis has not been explored. Our study was designed to analyze the expression and function of the CCL17-CCR4 axis in OLP. Methods:The mRNA expression levels of CCL17 and CCR4 in the circulating T cells of OLP subjects were examined by quantitative real-time PCR. The protein levels of CCL17 and CCR4 in the peripheral blood of OLP subjects were detected by enzyme-linked immunosorbent assay (ELISA) and Simple Western assay, respectively.The functional relevance of increased expression of CCL17 and CCR4 in OLP was demonstrated in proliferation, apoptosis, and migration assays. Results:The mRNA and protein expression levels of CCL17 and CCR4 in the peripheral blood of patients with OLP were significantly upregulated compared with those of controls. CCL17 induced the migration of OLP T cells. In addition, blocking CCR4 with a small molecule CCR4 antagonist not only inhibited the proliferation and migration of OLP T cells but also promoted the apoptosis of OLP T cells. Conclusion:Our findings indicate that the CCL17-CCR4 axis might be responsible for the inflammatory infiltration of T cells in OLP. K E Y W O R D SC-C chemokine receptor type 4, C-C motif chemokine ligand 17, oral lichen planus, T cells

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“…-Search strategies The PubMed (MEDLINE) database of the United Finally, 28 studies were evaluated. Of the 28 articles evaluated, 14 articles evaluated the IL-4 levels in the different samples, which are detailed in Table 1 (12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25); nine articles evaluated the effect of different factors on the production of IL-4 that also shown in Table 2 (26)(27)(28)(29)(30)(31)(32)(33)(34). One article examined the polymorphism of the IL-4 gene in patient with lichen planus, one article about the amount of IL-4 producing cells; one article examined the effect of IL-4 on CD 275+ cells and one article compared IL-4+ T cells levels between OLP and SCC specimen.…”

Section: Methodsmentioning

confidence: 99%

Role of interleukin-4 in pathogenesis of oral lichen planus: A systematic review

Sp¹,

Motahari²,

Fp³

et al. 2020

Med Oral

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Background: Oral lichen planus (OLP) is a premalignant mucocutaneous disease that affects 1-2% of the adult population. Immunological factor may act as etiological factor. The cellular immune cells such as T cells are important in pathogenesis of OLP. Interleukin-4 (IL-4) is secreted by T-helper 2 (Th2). Several studies have been carried out on the role of IL-4 in OLP. The aim of this study was to review the level of IL-4 in OLP, effective factors in the production of IL-4 and its role in the development of OLP. Material and Methods: A search in PubMed was performed on the literature published from 2000 until august 2019 using the following keywords: "oral lichen planus" or "OLP" and "interleukin-4" or "IL-4". Results: Originally, 37 articles were considered, of which 28 case-control articles were selected according to the inclusion/exclusion criteria. Conclusions: This review study shows that IL-4 plays a key role in the development of OLP. According to the past studies, there are several factors contributing to the production of this cytokine. Identification of the routes of production of IL-4 and its role in OLP might be useful for development of new preventive and therapeutic methods in management of patients with OLP.

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Myeloid dendritic cells stimulated by thymic stromal lymphopoietin promote Th2 immune responses and the pathogenesis of oral lichen planus

Cited by 28 publications

References 23 publications

Oral lichen planus: A disease or a spectrum of tissue reactions? Types, causes, diagnostic algorhythms, prognosis, management strategies

Oral lichen planus: A disease or a spectrum of tissue reactions? Types, causes, diagnostic algorhythms, prognosis, management strategies

Potential roles of the CCL17‐CCR4 axis in immunopathogenesis of oral lichen planus

Role of interleukin-4 in pathogenesis of oral lichen planus: A systematic review

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