Alopecia areata.

Abstract

The pathogenesis of organ specific, cell mediated autoimmune alopecia areata (AA) has substantially progressed in the last decade. These advances are partly based upon advances in immunology and genetics, improved technological methodology in RNA, DNA, proteomics, and computer analyses, as well as the development of the C3H/HeJ mouse model of AA. The discovery that full thickness skin grafts transfer AA from C3H/HeJ mice that spontaneously develop AA to multiple non-affected C3H/HeJ mice greatly shortened the time of AA onset and provided many more affected mice in this highly reproducible model of AA. These methodological and genetic advances combine to form practical bases for identifying subtypes of human and mouse AA, characterizing disease mechanisms, improving currently available treatments, and developing new, more effective therapies. In the next decade even more exciting new insights into the pathogenesis of subtypes of human AA, their genetic bases, and therapy development will become available based on in-depth data on specific gene mutations and signaling pathways involved. Other organ specific autoimmune diseases will surely benefit from the rapid progress in understanding AA.