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INTRODUCTION
Vitiligo is a chronic skin disorder characterized by progressive loss of functional melanocytes, which results in depigmentated macules in skin, hair and mucous membrane. It affects approximately 1% of the general population, with the disease beginning before the age of 20 in 50% of cases [1]. The disease is classified according to its extent and distribution, and can be subdivided into generalised or localised. In both types, the melanocytes are destroyed, resulting in loss of pigment from circumscribed areas of the skin. Although several theories have been proposed to explain the loss of melanocytes in vitiligo, the etiopathogenesis of the disease is still unclear. The clinical association with autoimmune disorders and organ specific antibodies indirectly support the idea of an autoimmune pathogenesis of the disease. In addition, many studies have indicated a role for both cellular and humoral immunity in the pathogenesis of vitiligo [2,3]. At the site of depigmentation, T cell infiltrates are invariably seen in patients with active vitiligo, along with a high frequency of cytotoxic T lymphocytes specific for melanocytic antigens, suggesting a direct melanocyte specific T cell attack [4]. Furthermore, many patients with vitiligo have serum auto antibodies directed against melanocytes. How antibodies to pigment cells arise, in vitiligo patients, has not yet been elucidated. They might result from a genetic predisposition to immune dysregulation at T or B cell levels. Involvement of the immune system in the pathogenesis is evidenced by the effectiveness of immunomodulatory agents, such as, corticosteroids and calcineurin inhibitors [5].
In 1956, anti-thyroglobulin antibody (anti-Tg) was first demonstrated as an auto antibody in the serum of patients with Hashimoto’s thyroiditis [6], and this finding first established the concept of organ-specific autoimmune disease. It has been known for some time that anti-Tg shows direct cytotoxic and cell destruction activity and maintain the thyroid autoimmune process over time, promoting the presentation of anti-Tg to T-cells by B-cells with antigen-presenting function [7]. Anti-Tg also promotes the proliferation of CD4-positive B- and T-lymphocytes in response to thyroglobulin [8]. These effects seem to be directly correlated with autoantibody concentration, and open up a new scenario regarding the role of B-cells with antigen-presenting function, in autoimmune thyroid disease, and new therapeutic possibilities for autoimmune diseases.
In the past, several authors described an...