The role of tyrosinase in autoimmune vitiligo

A single-nucleotide polymorphism in the gene encoding lymphoid protein tyrosine phosphatase (PTPN22) confers susceptibility to generalised vitiligo

“…The frequent association of vitiligo with autoimmune disorders and the demonstration of autoantibodies to melanosomal proteins in the serum of patients with the disease support this theory. [2][3][4][5][6] In addition, autoreactive CTLs, which specifically recognise melanocyte differentiation antigens, have been detected in both the peripheral blood and perilesional skin of individuals with vitiligo. [7][8][9] Melanocyte-specific CTLs have also been identified in patients with melanoma where vitiligo has occurred during immunotherapy and the adoptive transfer of melanoma antigen-specific CTLs may be associated with the regression of melanoma metastases and the appearance of vitiligo.…”

“…1 Support for this theory arises from the frequent association of vitiligo with autoimmune disorders and the demonstration of autoantibodies to melanosomal proteins in the serum of patients with the disease. [2][3][4][5][6] More recently, autoreactive cytotoxic T lymphocytes (CTLs), which specifically recognise melanocyte differentiation antigens, have been detected in both the peripheral blood and perilesional skin of individuals with vitiligo. [7][8][9] Furthermore, several genes that have a role in regulating immunity have been associated with susceptibility to vitiligo including: polymorphic markers in the cytotoxic T lymphocyte antigen-4 (CTLA-4) gene, the autoimmune susceptibility loci AIS1, AIS2, AIS3 and SLEV1 and certain human leukocyte antigen specificities of the major histocompatibility complex.…”

Genes of the LMP/TAP cluster are associated with the human autoimmune disease vitiligo

“…12,13 Two principal hypotheses concerning the etiology of vitiligo include: (1) the self-destruct model, which suggests that biochemical and/or structural defects inherent to patient melanocytes contribute to the initiation and/or progression of melanocyte cytolysis; and (2) the autoimmune model, which suggests that melanocyte death occurs through inappropriate immune system destruction of pigment cells. 11,14 There is considerable evidence that disease progression in some vitiligo patients involves autoimmune attack of the melanocytes, as evidenced by the presence of both cellular [15][16][17] and humoral [18][19][20] antimelanocyte autoimmune responses.…”

Induction of melanoma-associated antigen systemic immunity upon intratumoral delivery of interferon-γ retroviral vector in melanoma patients

“…21 Autoimmunity or melanoma/melanocyte destruction has been associated with specific anti-MAA Ab responses. 21,31,32 It is becoming more evident that treatment efficacy correlations are associated with Ab responses to specific MAA. We selected these specific MAA based on previous responses observed in melanoma patients; however, Ab to other types of MAA may also be as informative of response.…”