Implications of Th1 and Th17 cells in pathogenesis of oral lichen planus.
10.1007/s11596-012-0078-7
- Author:
Sanxiang XIE
1
;
Lei DING
;
Zhigang XIONG
;
Shengrong ZHU
Author Information
1. Department of Stomatology, Huazhong University of Science and Technology, Wuhan, China. xisix@163.com
- Publication Type:Journal Article
- MeSH:
Child;
Female;
Humans;
Interferon-gamma;
immunology;
Interleukin-17;
immunology;
Lichen Planus, Oral;
immunology;
pathology;
Male;
Middle Aged;
Th1 Cells;
immunology;
Th17 Cells;
immunology
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2012;32(3):451-457
- CountryChina
- Language:English
-
Abstract:
Oral lichen planus (OLP) is considered a T cell-mediated autoimmune disease with unknown aetiology. T helper cells appear to play an important role in the pathogenesis of OLP. We investigated the possible role of T helper cells, Th1 and Th17, in the lesions and circulation of patients with OLP. Forty patients with OLP and 15 healthy volunteers were recruited. Double immunofluorescence staining was used to detect Th1 and Th17 cells in the OLP lesions, and intracellular cytokine staining and flow cytometry to evaluate the proportion of Th1 and Th17 cells in peripheral blood. The levels of serum interferon (IFN)-γ and interleukin (IL)-17 were assessed by using an enzyme-linked immunosorbent assay. It was found that Th17 cells, as well as Th1 cells, were present in OLP lesions. The proportion of peripheral Th1 and Th17 cells was significantly increased in patients with OLP. The proportion of Th17 cells in atrophic-erosive OLP was elevated as compared with that in reticular OLP. Serum IL-17 levels in OLP patients were significantly higher than in controls, and those in the atrophic-erosive OLP group were increased as compared with the reticular OLP group. However, the levels of serum IFN-γ were slightly decreased in OLP patients. Our data suggested that Th1 and Th17 cells in the local lesions and peripheral blood may be associated with the pathogenesis of OLP, and that IL-17 may be an important proinflammatory cytokine in OLP. These findings enhance our understanding of OLP pathogenesis.
