Volume 15 Supplement 2
In vitroeffect of immune regulatory cytokines on vitiligo pathogenesis
© Singh et al; licensee BioMed Central Ltd. 2014
Published: 2 April 2014
Vitiligo is an acquired, hypomelanotic skin disorder characterized by circumscribed de-pigmented macules resulting from the loss of functional melanocytes. Various factors which may be responsible for precipitating this disorder in susceptible patients are oxidative stress, auto-immunity and neurochemicals.
Materials and methods
The skin samples were obtained with the consent of healthy individuals. Isolation of melanocytes was done according to the standard method  and normal human melanocytes (NHM) were grown in basal medium supplemented with growth factors. Dose dependent effect of different cytokines such as TNFα, IL6 and IL10 on NHM growth and proliferation was studied. MTT assay, RNA isolation, cDNA synthesis and relative gene expression studies were performed as described. This study was approved by the Institutional Ethical Committee for Human Research (IECHR), The M. S. University of Baroda, Vadodara, Gujarat, India.
The present study reveals that TNFα significantly induces IL6, ICAM1, TNFR1 and TNFR2 expression. In addition IL6 also induces ICAM1 expression . ICAM1 enhances T-cell and melanocyte attachment, thus augmenting melanocyte destruction by immune system. Under oxidative stress, which mimics the microenvironment of vitiligo, TNFA is found to enhance apoptosis of melanocytes which would result in de-pigmentation of the skin. Thus, our in vitro studies further strengthen the scientific evidences linking oxidative stress and immune system to vitiligo pathogenesis giving credence to a convergent terminal pathway of oxidative stress-autoimmunity mediated melanocyte loss.
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