Abstract
BackgroundVitiligo is an acquired hypomelanotic autoimmune disorder characterized by depigmented macules on the skin. Oxidative stress acts as an initial trigger and autoimmunity leads to vitiligo progression. Cytokines are key mediators of immune system and imbalance between pro- and anti-inflammatory cytokines play a vital role in the pathogenesis of autoimmune diseases. Also, relationship between oxidative stress and oxidative stress induced cytokine secretion is well established. Therefore, the present study aimed to monitor the expression levels of selected cytokine genes (IL1A, IL4, IL1R1, IL1RN and IFNG) from vitiliginous skin along with the effect of oxidative stress on in vitro cultured normal human melanocyte (NHM). MethodsThe gene expression of IL1A, IL1R1, IL1RN, IL4 and IFNG was performed by real-time PCR. Effect of oxidative stress on NHM was measured by MTT assay upon H2O2 treatment. ResultsOutcome of the study revealed significant increase in IFNG transcript levels from the non lesional and lesional skin of vitiligo patients as compared to controls (p = 0.0045 and p = 0.0198, respectively). However, no significant differrence was observed in the transcript levels of IL1A, IL4, IL1R and IL1RN from non lesional and lesional skin of vitiligo patients as compared to controls (p > 0.05). A significant decrease in melanocyte viability was observed upon H2O2 treatment in a dose dependent manner (p < 0.0001). ConclusionThe increased IFNG expression in vitiliginous skin advocates IFN-γ associated melanocyte destruction in vitiligo and decreased melanocyte viability upon H2O2 treatment suggests the vulnerability of melanocytes to oxidative stress which persists in vitiligo microenvironment.
Published Version
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