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Demonstration of autoantibodies against tyrosine hydroxylase in patients with alopecia areata
Author(s) -
Kemp E.H.,
Sandhu H.K.,
Weetman A.P.,
McDonagh A.J.
Publication year - 2011
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1111/j.1365-2133.2011.10597.x
Subject(s) - alopecia areata , autoantibody , antibody , tyrosinase , melanocyte , medicine , immunology , immune system , endocrinology , biology , enzyme , cancer research , biochemistry , melanoma
Summary Background There is strong evidence to suggest that alopecia areata (AA) is a tissue‐specific, T cell‐mediated autoimmune disease, which is usually characterized by patchy areas of hair loss on the scalp. Tyrosine hydroxylase (TH) is a known B‐cell autoantigen in patients with autoimmune polyendocrine syndrome type 1 (APS1) associated with the presence of AA. In addition, melanocyte‐specific proteins, gp100 and MelanA, are putative T‐cell autoantigens in AA and so may also represent targets of the humoral immune response. Objective To analyse the sera of patients with AA for the presence of antibodies against TH and the melanocyte‐specific proteins tyrosinase, tyrosinase‐related protein (TRP)‐1, TRP‐2, gp100 and MelanA. Methods Radioimmunoassays were used to detect the relevant antibodies in sera from patients with AA ( n = 32) and in sera from healthy individuals ( n = 28). Results Of 32 patients with AA, six (19%) were positive for TH antibodies. A significant increase in the frequency of TH antibodies in the AA patient group was evident when compared with controls ( P = 0·03). Only three of 32 (9%) patients exhibited antibody responses to tyrosinase, TRP‐1, TRP‐2 and gp100. No immunoreactivity against MelanA was detected in any patient with AA. Conclusion Antibodies against TH can be present in patients with AA unrelated to APS1. Humoral immune responses against tyrosinase, TRP‐1, TRP‐2, gp100 and MelanA are not prevalent in patients with AA. Overall, a dominant melanocyte‐specific B‐cell autoantigen in AA has yet to be identified.