Alopecia areata: an autoimmune disease?

被引:88
作者
McElwee, KJ
Tobin, DJ
Bystryn, JC
King, LE
Sundberg, JP
机构
[1] Jackson Lab, Bar Harbor, ME 04609 USA
[2] Univ Bradford, Dept Biomed Sci, Bradford BD7 1DP, W Yorkshire, England
[3] NYU, Skin Dis Res Ctr, Dept Dermatol, New York, NY USA
[4] Vanderbilt Univ, Div Dermatol, Nashville, TN USA
[5] Vet Adm Med Ctr, Nashville, TN 37203 USA
关键词
hypothesis; inflammation; disease model; rodent;
D O I
10.1111/j.1600-0625.1999.tb00385.x
中图分类号
R75 [皮肤病学与性病学];
学科分类号
100206 ;
摘要
A wide range of hypotheses such as focal infection, trophoneuroses, and endocrine dysfunction, have been previously proposed to explain the pathogenesis of alopecia areata (AA). Currently, the most widely held belief is that AA is an autoimmune disease with cellular; and/or humoral immunity directed against anagen hair follicle antigen(s). However, until recently evidence in support of an autoimmune mechanism of AA has been largely circumstantial. More fundamental evidence has recently been amassed in support of AA as an autoimmune disease by using animal models. These data include: 1) identification of cross-species hair follicle specific IgG autoantibodies, 2) The ability to induce AA in an animal model with transfer of skin from affected to naive individuals, and 3) the induction of disease by transfer of lymphocytes to human skin grafted to severe combined immunodeficiency mutant mice. A review of the previous and current data related to the autoimmune basis of AA is provided to put into perspective the future studies needed to definitively determine whether AA is an autoimmune disease.
引用
收藏
页码:371 / 379
页数:9
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