Expert Reviews in Molecular Medicine: http://www.expertreviews.org/
Accession information: Vol. 8; Issue 14; 20 June 2006 Abstract
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Model for pathogenesis of alopecia areata

Wei Lu, Jerry Shapiro, Mei Yu, Armin Barekatain, Blanche Lo, Andreas Finner and Kevin McElwee

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Figure 2. Model for pathogenesis of alopecia areata. The apparent immune-privileged status of anagen-stage hair follicles is thought to break down during AA, thereby exposing normally sequestered hair-follicle-specific antigens. Activated antigen-presenting cells (APCs) capture and process hair follicle antigens and present them in the context of major histocompatibility complex (MHC) class I and II. Antigen presentation, in association with costimulation and pro-inflammatory cyctokines, promotes the activation and proliferation of pathogenic, autoreactive T cells. T cells migrate to the skin and infiltrate around anagen-stage hair follicles, where a chemotactic stimulus is present. Peri-follicular inflammation disrupts hair follicle keratinocyte cells through cytokines whereas intrafollicular penetration enables cell–cell contact disruption of hair growth. The initial inflammation event increases hair follicle dystrophy and promotes continued pathogenic cell recruitment to perpetuate the autoimmune disease cycle. Hair follicles in a dystrophic state respond by truncating anagen and entering a telogen state. Any attempt to re-enter a new anagen growth phase is met with a renewed inflammatory response. Abbreviations: B, B cell; Tc, T cytotoxic cell; Th, T helper cell.

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