IL17A polymorphism and elevated IL17A serum levels are associated with oral lichen planus

IL17A polymorphism and elevated IL17A serum levels are associated with oral lichen planus INTRODUCTIONOral lichen planus (OLP) is a mucocutaneous T cell‐mediated chronic inflammatory disease of unknown aetiology. Mouth lesions have six clinical presentations, including reticular, papular, plaque‐like, erosive, atrophic and bullous, being the presence of white striae a clinical hallmark of the disease (van der Meij, Schepman, & van der Waal, ; Roopashree et al., ). Microscopically, it is characterised by a dense band‐like subepithelial lymphocytic infiltration and degeneration of basal keratinocytes, in a process orchestrated by T cells (Sugerman et al., ). In this context, cytotoxic CD8+ T cells are observed adjacent to basal keratinocytes and inside the epithelium while CD4+ T cells are shown to be present in the lamina propria. Besides, the lesional epithelium shows a higher concentration of Langerhans cells (LC), which are responsible for processing and presenting antigen derived to T cells and promote its activation (Gueiros et al., ). In this scenario, CD8+ cytotoxic T cells lead to keratinocyte apoptosis and consequent basal membrane disruption in a process regulated by CD4+ T cells through the promotion of an altered cytokine profile (Roopashree et al., ; Xie, Ding, Xiong, & Zhu, ).Recent evidence supports a central role of immune dysregulation in the pathogenesis of OLP (Lu, Zhang, Sun, Du, & http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Oral Diseases Wiley

IL17A polymorphism and elevated IL17A serum levels are associated with oral lichen planus

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Publisher
Wiley Subscription Services, Inc., A Wiley Company
Copyright
Copyright © 2018 John Wiley & Sons A/S. Published by John Wiley &Sons Ltd
ISSN
1354-523X
eISSN
1601-0825
D.O.I.
10.1111/odi.12718
Publisher site
See Article on Publisher Site

Abstract

INTRODUCTIONOral lichen planus (OLP) is a mucocutaneous T cell‐mediated chronic inflammatory disease of unknown aetiology. Mouth lesions have six clinical presentations, including reticular, papular, plaque‐like, erosive, atrophic and bullous, being the presence of white striae a clinical hallmark of the disease (van der Meij, Schepman, & van der Waal, ; Roopashree et al., ). Microscopically, it is characterised by a dense band‐like subepithelial lymphocytic infiltration and degeneration of basal keratinocytes, in a process orchestrated by T cells (Sugerman et al., ). In this context, cytotoxic CD8+ T cells are observed adjacent to basal keratinocytes and inside the epithelium while CD4+ T cells are shown to be present in the lamina propria. Besides, the lesional epithelium shows a higher concentration of Langerhans cells (LC), which are responsible for processing and presenting antigen derived to T cells and promote its activation (Gueiros et al., ). In this scenario, CD8+ cytotoxic T cells lead to keratinocyte apoptosis and consequent basal membrane disruption in a process regulated by CD4+ T cells through the promotion of an altered cytokine profile (Roopashree et al., ; Xie, Ding, Xiong, & Zhu, ).Recent evidence supports a central role of immune dysregulation in the pathogenesis of OLP (Lu, Zhang, Sun, Du, &

Journal

Oral DiseasesWiley

Published: Jan 1, 2018

Keywords: ; ; ;

References

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