T lymphocytes and altered keratinocytes express interferon-γ and interleukin 6 in lichen planus

Abstract

Lichen planus is assumed to represent a delayed hypersensitivity reaction, in the course of which cytokines control the proliferation and differentiation of cytotoxic T lymphocytes which attack the epidermis and cause apoptosis of undifferentiated keratinocytes. Since interferon-gamma and interleukin 6 are known to be markedly generated in lichen planus, we investigated the cellular localization of these cytokines in affected skin/oral mucosa biopsy specimens using in situ hybridization for interferon-gamma and in situ reverse transcription-polymerase chain reaction for interleukin 6 mRNA. In the upper subepithelial connective tissue interferon-gamma mRNA was noted within proliferating CD3+ T lymphocytes. In this tissue compartment interleukin 6 mRNA was detected in infiltrating CD4+ and CD8+ T lymphocytes. In the epithelium, expression of interferon-gamma mRNA and interleukin 6 mRNA was observed in the basal and suprabasal keratinocytes of altered skin/oral mucosa. In contrast, normal skin did not reveal any interferon-gamma or interleukin 6 expression, although a few CD4+ and CD8+ T lymphocytes were noted in the dermis as well as the epidermis. These findings indicate that in lichen planus the proinflammatory cytokines interferon-gamma and interleukin 6 are produced not only by activated T lymphocytes but also by altered keratinocytes, and suggest that stimulated keratinocytes may amplify the course of lichen planus.

IFN-Gamma and IL-4 in Saliva of Patients with Oral Lichen Planus: A Study in an Ethnic Chinese Population

“…Fayyazi et al observed the expression of IFN-γ mRNA and interleukin 6 mRNA in the basal and suprabasal keratinocytes of altered skin/oral mucosa [35]. Simark-Mattsson et al found that there were cells expressing mRNA for IL-2, IL-4, IL-10, TNF-α and TGF-β1 in all OLP lesions.…”

Possible Role of TNF-α, IFN-γ, FAS/APO1 in the Etiopathogenesis of Lichen Planus

“…They also demonstrated that proinflammatory cytokines such as IFN-γ and IL-6 were produced not only in active T lymphocytes but also in keratinocytes in basal and suprabasal layers [28]. They reported that TNF-α and IFN-γ may lead to liquefaction degeneration in basal membrane and basal keratinocytes.…”

The Role of Salivary Cytokines in Patients with Oral Lichen Planus

“…Gu et al [4] detected elevated levels of oral and serum IL-6 in patients with ulcerative lichen in comparison to the reticular lichen and controls thus suggesting that elevated IL-6 might reflect chronic inflammatory nature of ulcerative lichen. On the contrary, Fayyazi et al [5] suggested that OLP is a delayed type of hypersensitivity reaction in which cytokines (including IL-6) control proliferation and differentiation of cytotoxic Tlymphocytes which attack epidermis and lead to apoptosis of undifferentiated keratinocytes. Last but not least Rhodus et al [6] reported that patients with oral squamous cell carcinoma have elevated salivary IL-6 and TNF-α in comparison to the patients with precancerous lesions and healthy controls.…”