What is the proposed autoimmune pathophysiology of alopecia areata?

Updated: Jun 07, 2018
  • Author: Chantal Bolduc, MD, FRCPC; Chief Editor: Dirk M Elston, MD  more...
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Answer

Much evidence supports the hypothesis that alopecia areata is an autoimmune condition. The process appears to be T-cell mediated, but antibodies directed to hair follicle structures also have been found with increased frequency in alopecia areata patients compared with control subjects. Using immunofluorescence, antibodies to anagen-phase hair follicles were found in as many as 90% of patients with alopecia areata compared with less than 37% of control subjects. The autoantibody response is heterogeneous and targets multiple structures of the anagen-phase hair follicle. The outer root sheath is the structure targeted most frequently, followed by the inner root sheath, the matrix, and the hair shaft. Whether these antibodies play a direct role in the pathogenesis or whether they are an epiphenomenon is not known.

Histologically, lesional biopsy findings of alopecia areata show a perifollicular lymphocytic infiltrate around anagen-phase hair follicles. The infiltrate consists mostly of T-helper cells and, to a lesser extent, T-suppressor cells. CD4+ and CD8+ lymphocytes likely play a prominent role because the depletion of these T-cell subtypes results in complete or partial regrowth of hair in the Dundee experimental bald rat (DEBR) model of alopecia areata. The animals subsequently lose hair again once the T-cell population is replete. The fact that not all animals experience complete regrowth suggests that other mechanisms likely are involved. Total numbers of circulating T lymphocytes have been reported at both decreased and normal levels.


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