Detailed Description:

The pathogenesis of vitiligo is still unclear but some theories can explain it such as oxidative stress, autoimmunity, autocytotoxicity, genetic factors, neural and melanocytorrhagy . Loss of pigment which occur in vitiligo may be due to two main causes: absence of melanocytes and/or the inability of melanocytes to produce and store melanin in melanosomes in the process of melanogenesis. High mobility group box protein B1 (HMGB1) normally presents in the nucleus to maintain genomic stabilization and regulate gene transcription. but, HMGB1 can be released outside the cell due to exposure to stressful factors such as oxidative stress and function as a damage-associated molecular pattern (DAMP) protein leading to strong proinflammatory effects. Recent data showed that HMGB1 is overexpressed in both blood and lesional specimens from vitiligo patients. Moreover, oxidative stress triggers the release of HMGB1 from keratinocytes and melanocytes, indicating that HMGB1 may participate and play a crucial role in the pathological process of vitiligo. HMGB1 Directly induces Melanocyte apoptosis through stimulation with reactive oxidative stress (ROS) or ultraviolet B (UVB) in vitro which significantly increases the release of HMGB1 from keratinocytes, which inhibits the expression of melanogenesis-related molecules such as microphthalmia- associated transcription factor (MITF), tyrosinase-related proteins and the gp100 protein in a paracrine manner and finally activate caspase-3 to trigger melanocyte apoptosis}}