Cytokine pathways and interactions in alopecia areata

This is the authors' abstract. We don't add key points for this paper.

Alopecia areata (AA) is an autoimmune disease resulting in the premature arrest of the follicular growth cycle clinically resulting in patchy, non-scarring hair loss. The presence of a dense follicular T cell infiltrate and variations in cytokines have led to the hypothesis that T cell activation and alterations in inflammatory mediators are crucial participants in the etiopathogenesis of the disease. Various studies suggest that the AA pathogenesis has a dominant TH1-mediated component, with potential involvement of the TH17 pathway. However, a fully integrated view of intersecting cytokine networks that support the autoimmune response in AA is lacking. A more precise understanding of cytokine pathways in disease is required to rationally explore cytokine targeted treatment strategies. Here, we comprehensively and critically review the current literature to provide a working framework regarding the complexity of T cell-cytokine interactions in AA, emphasizing the areas necessitating further research, particularly for the development of novel therapeutic options.