Oral lichen planus: an immunohistochemical study of heat shock proteins (HSPs) and cytokeratins (CKs) and a unifying hypothesis of pathogenesis

Chaiyarit, Ponlatham; Kafrawy, Abdel H.; Miles, Dale A.; Zunt, Susan L.; Dis, Margot L. Van; Gregory, Richard L.

doi:10.1111/j.1600-0714.1999.tb02026.x

Cited by 54 publications

(41 citation statements)

References 26 publications

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“…Proposed activation/tolerance theories regarding dendritic cells-i.e., that stimulatory function is either enhanced by toll-like receptors on dendritic cells recognizing microbial products and upregulating costimulatory molecules (47) or that damage in other cells and production of molecules such as heat shock proteins act as "danger signals" (48) that activate dendritic cells-may also be true for epithelial cells (49)(50)(51)(52).…”

Section: Discussionmentioning

confidence: 99%

Immune receptors CD40 and CD86 in oral keratinocytes and implications for oral lichen planus

et al. 2017

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Lichen planus (LP) is a chronic T-cell-mediated mucocutaneous inflammatory disease that targets stratified epithelia, including those lining the oral cavity. The intraoral variant of LP (OLP) is associated with interferon (IFN)-γ production by infiltrating T lymphocytes; however, the role of epithelial cells in the etiopathogenesis OLP is not completely understood. There is however a growing body of evidence regarding the involvement of epithelial-derived cytokines, immune receptors, and costimulatory molecules in the pathobiological processes that promote and sustain OLP. In the present study, we used a reverse transcriptase-polymerase chain reaction assay to assess whether CD40-a receptor found mainly on antigen presenting cells-and the costimulatory molecule CD86 were expressed in oral keratinocytes (three strains of primary normal oral keratinocytes and the H357 cell line) in the presence or absence of IFN-γ. To further characterize the involvement of CD40 in OLP, expression and distribution of receptor and ligand (CD40/CD154) in tissues from OLP were evaluated by immunohistochemistry. The present results are the first to show that both CD40 and CD86 are constitutively expressed at low levels in oral keratinocytes and that their expression was enhanced by IFN-γ stimulation. The intensity of CD40 staining in OLP tissues was strong. Taken together, the results strongly suggest that CD40 and CD86 play a role in the pathophysiology of oral inflammatory diseases such as OLP.

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Section: Discussionmentioning

confidence: 99%

Immune receptors CD40 and CD86 in oral keratinocytes and implications for oral lichen planus

et al. 2017

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“…8,11 Overexpression of HSPs has been observed in certain cancers (breast, uterine cervix, lung, pancreas, ovary, liver, leukaemia, and oral cavity). [3][4][5][6]12,13 The physiopathologic activity of HSPs in tumorogenes not known, but it is related to cell growth and differentiation, and has been associated with the mutant form of the tumor suppressor gene TP53. 3,12,[14][15][16][17][18] Moreover, experimental evidence suggests that HSPs may promote tumorogenesis by suppressing apoptosis.…”

mentioning

confidence: 99%

Heat Shock Proteins (HSP70 and HSP27) as Markers of Epithelial Dysplasia in Oral Leukoplakia

Seoane

Varela‐Centelles²,

Ramírez³

et al. 2006

The American Journal of Dermatopathology

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Heat shock proteins (HSPs) play a significant role in cell proliferation, differentiation, and oncogenesis. HSP70 and HSP27 are constitutively and gradually expressed in a broad range of normal tissues and neoplasms, and their expression has been assessed as markers for oral epithelial dysplasia. The study involved 43 patients with oral leukoplakia (OL): 23 were categorized as nondysplastic and 20 as dysplastic OLs. Immunohistochemistry was carried out with the monoclonal antibodies HSP70 and HSP27. The presence of epithelial dysplasia and its histologic grading was evaluated according to the World Health Organization classification: mild, moderate, and severe squamous epithelial dysplasia. Expression of HSPs within the epithelium was also evaluated. The difference in the percentage of HSP70 positive nuclei in nondysplastic and dysplastic OL reached statistical significance(Equation is included in full-text article.)95% confidence interval = 17.74-43.82; P = 0.000). None of the 43 specimens analyzed showed positive nuclear immunostaining for anti-HSP27 antibody. No significant difference for HSP27 cytoplasmic expression could be identified between OL with or without epithelial dysplasia(Equation is included in full-text article.)95% confidence interval = 0.44-3.95; P = 0.89). It is concluded that the nuclear HSP70 immunoexpression could be an objective marker for the presence of the epithelial dysplasia in OL.

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“…A semiquantitative way of immunohistochemical evaluation presented by Chaiyarit et al [9,33] was used to assess expression of TLR2, 4, and 9. The epidermis was divided into basal layer, suprabasal layer, and superficial layer under microscopic view and the proportion of immunoreactive cells and intensity of staining were assessed.…”

Section: Immunohistochemical Evaluationmentioning

confidence: 99%

Immunohistochemical study of toll-like receptors 2, 4, and 9 expressions in pemphigus and bullous pemphigoid lesions

2016

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Pemphigus and bullous pemphigoid (BP) are severe autoimmune skin diseases. Whether innate immunity could be a trigger or a part of the pathogeneses is unknown. Toll-like receptors (TLRs) are important components of the innate immune system, with no previous evaluation of TLRs in autoimmune bullous diseases. This work aims to investigate TLRs 2, 4, and 9 expressions in pemphigus and bullous pemphigoid. Thirty-six patients with pemphigus vulgaris (PV), pemphigus foliaceus (PF), bullous pemphigoid (BP), and six healthy controls were studied. Skin biopsies from the patients and the controls were examined immunohistochemically for TLR2, 4, and 9 expressions. The TLR4 expressed mainly at the basal layer of epidermis in controls, but in the cases with autoimmune bullous diseases, TLR4 staining located at basal layer and suprabasal layer, even superficial layer of epidermis. The immunostaining-intensity-distribution (IID) index of TLR4 in patients with PF (13.83, P = 0.001), PV (13.08, P = 0.003), and BP (11.42, P = 0.042) were significantly higher than that of the controls (6.17). TLR2 and TLR9 showed no significantly changes at epidermal expression (P > 0.05) compared with controls. There was no correlation found between the expressions of these TLRs. This work, thus, shows a re-localization of TLR4 expression sites with increased expression in pemphigus and bullous pemphigoid lesions. Targeting TLR4 signaling is expected to be a novel treatment strategy for autoimmune bullous diseases.

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Oral lichen planus: an immunohistochemical study of heat shock proteins (HSPs) and cytokeratins (CKs) and a unifying hypothesis of pathogenesis

Cited by 54 publications

References 26 publications

Immune receptors CD40 and CD86 in oral keratinocytes and implications for oral lichen planus

Immune receptors CD40 and CD86 in oral keratinocytes and implications for oral lichen planus

Heat Shock Proteins (HSP70 and HSP27) as Markers of Epithelial Dysplasia in Oral Leukoplakia

Immunohistochemical study of toll-like receptors 2, 4, and 9 expressions in pemphigus and bullous pemphigoid lesions

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