1. Skin Research Laboratory, The B. Rapaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel
2. ^*Department of Dermatology, SUNY at Stony Brook,New York, U.S.A.

Correspondence: Dr Richard S. Kalish, Department of Dermatology Health Sciences Center T-16, 060 SUNY at Stony Brook Technion, Stony Brook, NY, 11794-8165. Email: rkalish@epo.som.sunysb.edu

Received 23 December 1998; Revised 23 February 1999; Accepted 25 February 1999.

Abstract

Much evidence suggests that alopecia areata is a tissue restricted autoimmune disease. Alopecia areata responds to immunosuppressive agents, and is associated with other tissue restricted autoimmune diseases, including autoimmune thyroiditis and vitiligo. Furthermore, hair regrows when involved scalp is transplanted to nude mice. This study was undertaken to determine whether alopecia areata is mediated by T lymphocytes. Involved scalp from alopecia areata patients was grafted onto SCID mice. Additional biopsies from lesional scalp of the same patients were used to isolate T lymphocytes. These T lymphocytes were cultured with hair follicle homogenate, as well as autologous antigen presenting cells. The T lymphocytes were then injected into autologous scalp grafts on the SCID mice, which had regrown hair. Injection of scalp T lymphocytes resulted in hair loss. Hair loss was associated with the histologic and immunochemical changes of alopecia areata, including perifollicular infiltrates of T cells, along with HLA-DR and ICAM-1 expression by the follicular epithelium. Scalp T lymphocytes that had not been cultured with hair follicle homogenate did not have this effect. Preliminary data suggests hair loss requires a collaboration between CD8⁺and CD4⁺T cells. These studies have demonstrated that alopecia areata can be induced by the transfer of T cells that recognize a hair follicle auto-antigen.