Abstract

Recent studies have noticed significant role of interleukin (IL)-17, 22, 23, Foxp3, interferon-gamma (IFN-γ) and Wnt5a in oral and cutaneous lichen planus (LP). This study was undertaken to assess whether similar expression exists in lichen planus pigmentosus (LPP). We recruited 30 patients of treatment-naïve 'LPP' (in absence of cutaneous/mucosal LP elsewhere, group 1), 10 patients having active treatment-naïve cutaneous 'LP' (group 2), 10 patients having 'post-LP' hyperpigmentation (in absence of active LP and off treatment for at least past 3months, group 3), and 10 controls. Quantitative real-time polymerase chain reaction (qRT-PCR, peripheral blood mononuclear cells [PBMCs] and skin) and immunohistochemistry (IHC, skin) was performed. mRNA expression (in PBMCs) of IL-17A, IL-22, IL-23A, IFN-γ and Foxp3 was significantly decreased in group 1 and 3 as compared to group 2 (p < 0.05). Wnt5a expression was maximal in controls; and while there was no difference between group 1 and 2; whereas expression in group 3 was significantly lesser than group 1 and 2 (p < 0.05). qRT-PCR (skin) and IHC (skin) revealed similar results; and mRNA expression and mean fluorescence intensity of IL-17A, IL-22, IL-23A/R was significantly increased in group 2 and 3 compared to group 1 (p < 0.05). Mean fluorescence intensity and mRNA expression of IFN-γ, Foxp3 and Wnt5a were significantly increased in group 2 compared to group 1 (p < 0.05); whereas the difference between group 1 and 3 was not significant. Mean fluorescence intensity and mRNA expression of IL-17A, 1L-22 and IFN-γ showed no difference between group 2 and 3; whereas that of IL-23A/R, foxp3 and wnt5a were significantly higher in group 2 than group 3 (p < 0.05). Overall, maximal expression of IL-17A, IL-22, IL-23A, IFN-γ and Foxp3 (mRNA PBMCs) was observed in LP. Minimal expression of IL-17A, IL-22, IL-23A/R, IFN-γ and Foxp3 (mRNA skin and IHC skin) was seen in LPP patients. In contrast to LP, LPP lacks the expression of IFN-γ, Foxp3 and the cytokines representing Th17 pathway, and thus seems to have a distinct pathogenesis.

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