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Published on: February 18, 2015
Th1 cytokines in oral lichen planus
Ambereen Khan1, Camile S Farah, Neil W Savage
1Oral Biology and Pathology, The University of Queensland, St Lucia, Brisbane, Queensland, Australia.
Insights
Oral lichen planus (OLP) involves CD8+ T-cells and cytokines like interferon-gamma (IFN-γ) and tumor necrosis factor-alpha (TNF-α). These findings suggest a T helper 1 immune response promoting cytotoxic T-cell activity in OLP.
Area of Science:
- Immunology
- Oral Pathology
Background:
- Cell-mediated immunity in oral lichen planus (OLP) is influenced by cytokines and their receptors.
- Understanding these interactions is crucial for OLP pathogenesis.
Purpose of the Study:
- To investigate the role of cytokines and their receptors in cell-mediated immune responses in OLP.
- To characterize the immune cell infiltrate and cytokine expression profiles in OLP lesions.
Main Methods:
- In situ cytokine expression was analyzed using immunohistochemistry.
- In vitro cytokine secretion from OLP lesional T cells was assessed via ELISA.
- Immune cell populations were identified using CD markers (CD4+, CD8+).
Main Results:
- CD8+ T-cells were the predominant mononuclear cells in OLP lesions, with some adjacent to degenerating keratinocytes.
- IFN-γ and TNF-α were expressed by mononuclear cells and keratinocytes, with basal keratinocytes showing continuous TNF-α expression.
- OLP T-cells secreted IFN-γ in vitro, which was modulated by TNF-α stimulation; IL-4, IL-10, and TGF-β1 were not detected.
Conclusions:
- The data indicate a T helper 1 (Th1) immune response in OLP.
- This Th1 response may drive CD8+ cytotoxic T-cell activity, contributing to OLP development.
Background:
Cell-mediated immune responses in oral lichen planus (OLP) may be regulated by cytokines and their receptors.
Methods:
In situ cytokine expression and in vitro cytokine secretion in OLP were determined by immunohistochemistry and ELISA.
Results:
The majority of subepithelial and intraepithelial mononuclear cells in OLP were CD8+. In some cases, intraepithelial CD8+ cells were adjacent to degenerating keratinocytes. CD4+ cells were observed mainly in the deep lamina propria with occasional CD4+ cells close to basal keratinocytes. Mononuclear cells expressed IFN-gamma in the superficial lamina propria and TNF-alpha adjacent to basal keratinocytes. Basal keratinocytes expressed TNF-alpha as a continuous band. TNF R1 was expressed by mononuclear cells and basal and suprabasal keratinocytes. There was variable expression of TGF-beta1 in the subepithelial infiltrate while all intraepithelial mononuclear cells were TGF-beta1-. Keratinocytes in OLP stained weakly for TGF-beta1. Unstimulated OLP lesional T cells secreted IFN-gamma in vitro. TNF-alpha stimulation down-regulated IFN-gamma secretion and up-regulated TNF-alpha secretion. IL-4, IL-10 and TGF-beta1 secretion were not detected.
Conclusions:
These data suggest the development of a T helper 1 immune response that may promote CD8+ cytotoxic T-cell activity in OLP.
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