Autoimmune features of vitiligo

Vitiligo can be found in autoimmune families in association with Addison disease, alopecia areata, pernicious anemia, or mucocutaneous candidiasis, with an incidence 10-15 times higher than in the general population. Antibodies to thyroid, adrenal gland and gastric parital cells can be demonstrated in vitiligo patients; using modern techniques, antibodies reactive with melanocytes have been consistently-found in vitiligo patients' sera. The levels of these antibodies are greatest in patients with actively progressing disease and in vitiligo patients with other autoimmune disease. Both melanocyte-specific antibodies and antibodies reactive to other cells in addition to melanocytes have been identified. Some of these antibodies are specific for proteins involved in melanization such as tyrosinase and tyrosinase-related protein 1. Antibodies to a melanocyte-specific 85 kDa antigen have been described in dogs, cats and horses with vitiligo. Similar antibodies are found in a chicken model of vitiligo; bursectomv in these animals delays onset of vitiligo.

The functional significance of these autoantibodies was demonstrated when Norris and colleagues showed that cytotoxicity of cultured human melanocyte targets could be induced by antibodies in vitiligo patients' sera by either complement-mediated lysis or antibody-dependent cellular cytotoxicity (ADCC). Other investigators have subsequently verified that autoantibodies in vitiligo patients' sera can induce cytotoxic damage of melanocytes by multiple anti-body-dependent mechanisms. In a nude mouse model, injection of sera from vitiligo patients induced depigmentation of human skin grafted onto the nude mouse. Cytotoxicity induced by autoantibodies is the only proposed mechanism in vitiligo in which a specific factor isolated from vitiligo patients has been directly demonstrated to induce melanocyte destruction both in vitro and in vivo.

The factors inducing melanocyte destruction may differ in individual vitiligo patients. Members of autoimmune families are predisposed to produce autoantibodies, and melanocyte-specific autoantibodies are likely to be the major determinant of melanocyte cytotoxicity in these families. In other vitiligo patients it is possible that autoimmune melanocyte destruction may represent a later stage of disease, following melanocyte destruction by auto-cytotoxicity or other factors. However, once melan-ocyte-specific antibodies are produced, it is likely that these produce additional melanocyte damage and the depletion of melanocytes in the basal layer of the epidermis.

See also: Adrenal autoimmunity; Antibodies, specificity; Antibody-dependent cellular cytotoxicity; Antigens, cell surface; Autoimmune diseases; Cytotoxicity, mechanisms of; Polyendocrine autoimmunity; Skin, autoimmune diseases.

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