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  Indian J Med Microbiol
 

Figure 1: Proposed patho-mechanisms behind the convergence theory. Convergence theory proposes that the various triggers, perhaps, work in combination to bring about onset of vitiligo. (I) Genetic theory: In a genetically predisposed person, various environmental triggers such as UV radiation, stress and ROS bring about the onset of vitiligo. (II) Neurohumoral hypothesis: Stress brings about an increased secretion of catecholamines and neuropeptides leading to increased production of free radicals, which bring about damage to melanocytes and generation of neoantigens, thereby, triggering immune response. (III) Autocytotoxic hypotheses: Exposure to UV radiation leads to spontaneous production of ROS and increased HMGB1 (high-mobility group box 1) protein level, which brings about activation of caspases, and subsequent loss of melanocytes. (IV) Autoimmune hypothesis: Various triggers bring about synthesis of neoantigens, which initiate an autoimmune phenomenon. (V) Melanocytorrhagy: ROS, structural alterations in melanocytes and alterations in tenascin lead to loss of adhesion of melanocytes to the basement membrane which results in transepidermal elimination of melanocytes on exposure to mild trauma

Figure 1: Proposed patho-mechanisms behind the convergence theory. Convergence theory proposes that the various triggers, perhaps, work in combination to bring about onset of vitiligo. (I) Genetic theory: In a genetically predisposed person, various environmental triggers such as UV radiation, stress and ROS bring about the onset of vitiligo. (II) Neurohumoral hypothesis: Stress brings about an increased secretion of catecholamines and neuropeptides leading to increased production of free radicals, which bring about damage to melanocytes and generation of neoantigens, thereby, triggering immune response. (III) Autocytotoxic hypotheses: Exposure to UV radiation leads to spontaneous production of ROS and increased HMGB1 (high-mobility group box 1) protein level, which brings about activation of caspases, and subsequent loss of melanocytes. (IV) Autoimmune hypothesis: Various triggers bring about synthesis of neoantigens, which initiate an autoimmune phenomenon. (V) Melanocytorrhagy: ROS, structural alterations in melanocytes and alterations in tenascin lead to loss of adhesion of melanocytes to the basement membrane which results in transepidermal elimination of melanocytes on exposure to mild trauma