Alopecia areata is a disorder that results in non-scarring hair loss. The psychological impact can be significant, leading to feelings of depression and social isolation. The disease remains incurable though it has been studied for years. Available treatment options at best, are beneficial for milder cases, and the rate of relapse is high. Understanding the exact mechanisms of hair loss in alopecia areata is therefore of utmost importance to help identify potential therapeutic targets. The main theory of alopecia areata pathogenesis is that it is an autoimmune phenomenon resulting from a disruption in hair follicle immune privilege. What causes this breakdown is an issue of debate. Some believe that stressed hair follicle environment triggers antigen presentation while others blame a dysregulation in the central immune system to entangle the follicles. Evidence for the latter theory is provided by animal studies as well investigation around the AIRE gene. Different immune cell lines including plasmacytoid dendritic cells, natural killer cells, and T-cells along with key molecules such as IFNγ, IL-15, MICA, and NKG2D have been identified to contribute to the autoimmune process. In this article, we seek to review the pathophysiologic mechanisms proposed in recent years in a narrative fashion. This article is protected by copyright. All rights reserved.