Recent advances in the pathogenesis of autoimmune hair loss disease alopecia areata

Abstract

Alopecia areata is considered to be a cell-mediated autoimmune disease, in which autoreactive cytotoxic T cells recognize melanocyte-associated proteins such as tyrosinase. This review discusses recent advances in the understanding of the pathogenesis of alopecia areata, focusing on immunobiology and hormonal aspects of hair follicles (HFs). The HF is a unique "miniorgan" with its own immune and hormonal microenvironment. The immunosuppressive milieu of the anagen hair bulb modulated by immunosuppressive factors is known as "hair follicle immune privilege." The collapse of the hair follicle immune privilege leads to autoimmune reactions against hair follicle autoantigens. Alopecia areata is sometimes triggered by viral infections such as influenza that causes excess production of interferons (IFN). IFN- γ is one of the key factors that lead to the collapse of immune privilege. This paper reviews the interactions between the endocrine and immune systems and hair follicles in the pathogenesis of alopecia areata.

Figure 1

The pathogenesis of alopecia areata and treatment strategies. Environmental factors such as viral infections and bacterial superantigens may induce IFN-γ and CXCL10 expressions in the hair bulbs. Subsequently, autoreactive Th1 and Tc1 cells (blue circles) accumulate in and around hair bulbs—the so-called “swarm of bees.” Anagen-associated hair follicle (HF) autoantigens (orange circles) are recognized by Th1 and Tc1 cells, which lead to a secondary autoimmune phenomenon and resultant hair loss.