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06.07.2023 | Review

The potential roles of Th17 cells in the pathogenesis of oral lichen planus

verfasst von: Shima Afzali, Elham Mohammadisoleimani, Yaser Mansoori, Poopak Mohaghegh, Maryam Bahmanyar, Behnam Mansoori, Babak Pezeshki, Ghasem Nikfar, Alireza Tavassoli, Abbas Shahi, Ali Moravej

Erschienen in: Inflammation Research | Ausgabe 7/2023

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Abstract

Background

Oral lichen planus (OLP) is a T cell-mediated chronic autoimmune disease, whose pathogenesis and etiology are not entirely understood. OLP is characterized by subepithelial lymphocyte infiltration and elevated intra-epithelial lymphocytes. The majority of lamina propria lymphocytes are CD4⁺ T cells. CD4⁺ helper T (Th) cells play a crucial role in activating CD8⁺ cytotoxic T cells (CTLs) through interactions and cytokine production. Th1 and Th2 cells are well-accepted to be associated with OLP pathogenesis. However, OLP treatment is challenging yet, the more information we have about the pathology of OLP, the easier it will be treated. With the discovery of Th17 cells in recent years and the demonstration of their role in autoimmune disease, many researchers started to investigate the role of Th17 in the pathogenesis of OLP.

Methods

To make up this review, studies covering the role of TH17 in different types of lichen planus were selected from major databases.

Results

As we review in this article, Th17 cells and their signature cytokines play an important role in OLP pathogenesis. As well, utilizing some anti-IL-17 antibodies showed promising results in improving the disease; however, more studies are still needed to better understand and treat OLP.

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Titel: The potential roles of Th17 cells in the pathogenesis of oral lichen planus
verfasst von: Shima Afzali
Elham Mohammadisoleimani
Yaser Mansoori
Poopak Mohaghegh
Maryam Bahmanyar
Behnam Mansoori
Babak Pezeshki
Ghasem Nikfar
Alireza Tavassoli
Abbas Shahi
Ali Moravej
Publikationsdatum: 06.07.2023
Verlag: Springer International Publishing
Erschienen in: Inflammation Research / Ausgabe 7/2023
Print ISSN: 1023-3830
Elektronische ISSN: 1420-908X
DOI: https://doi.org/10.1007/s00011-023-01763-7

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