Alopecia areata: autoimmunity--the evidence is compelling.
There is strong evidence indicating that alopecia areata is a tissue-specific, autoimmune disease. Hair loss is associated with a perifollicular lymphocytic infiltrate made up primarily of CD4+ cells, along with a CD8+ intrafollicular infiltrate. Evidence of immune activation includes expression of HLA-DR; HLA-A,B,C; and ICAM-1 on the follicular epithelium. It is likely that the follicular expression of HLA-DR and ICAM-1 is induced by interferon-gamma produced by T cells. Antibodies to follicular epithelium are often present, but their significance is not known. Lesional scalp from alopecia areata patients grafted onto nude mice regrows hair coincident with a loss of infiltrating lymphocytes from the graft. Hair loss can be transferred to human scalp explants on SCID mice by injection of lesional T cells. It is necessary to activate the T cells by culture with follicular autoantigens. Melanocyte-associated antigens are also capable of activating T cells to induce hair loss, suggesting that they are capable of functioning as autoantigens for alopecia areata. Parallel evidence in rodent models of spontaneous alopecia areata also strongly supports a role for T cells in the pathogenesis of this condition.
Department of Dermatology, Health Sciences Center, State University of New York at Stony Brook, Stony Brook, New York 11794-8165, USA. richard.kalish@stonybrook.edu
Richard S
RS
Kalish
Amos
A
Gilhar
D000506:Alopecia Areata / Q000235:genetics* / Q000276:immunology* / Q000628:therapy; D000818:Animals; D001323:Autoantibodies / Q000032:analysis; D001327:Autoimmune Diseases / Q000235:genetics* / Q000276:immunology* / Q000628:therapy; D004195:Disease Models, Animal; D008040:Genetic Linkage; D018859:Hair Follicle / Q000276:immunology; D006801:Humans; D013601:T-Lymphocytes / Q000276:immunology
D001323:Autoantibodies