| First Author | Kalish RS | Year | 2003 |
| Journal | J Investig Dermatol Symp Proc | Volume | 8 |
| Issue | 2 | Pages | 164-7 |
| PubMed ID | 14582666 | Mgi Jnum | J:85976 |
| Mgi Id | MGI:2677625 | Doi | 10.1046/j.1087-0024.2003.00802.x |
| Citation | Kalish RS, et al. (2003) Alopecia areata: autoimmunity--the evidence is compelling. J Investig Dermatol Symp Proc 8(2):164-7 |
| abstractText | 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. |
