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For instance, these cells identify melanocytes via Major Histocompatibility Complex (MHC) class I molecules and induce apoptosis through the directed release of perforin and granzyme B, while IFN- secretion exacerbates local inflammation and amplifies the autoimmune response, constituting a key pathological event in vitiligo ( Recent research highlights that environmental factors, such as ultraviolet (UV) radiation or chemical exposure, can trigger vitiligo by inducing the production of pathogen-associated molecular patterns (PAMPs) or damage-associated molecular patterns (DAMPs) ( + T cells target melanocytes, resulting in skin depigmentation

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