The British journal of dermatology · 2011
Demonstration of autoantibodies against tyrosine hydroxylase in patients with alopecia areata.
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Kemp E H, Sandhu H K, Weetman A P, McDonagh A J
Аннотация
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.
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.