Alopecia areata is an autoimmune nonscarring hair loss characterized by peribulbar infiltrates of activated T cells and by degenerative changes in the hair follicle matrix that eventually result in alopecia. The cause of immune dysregulation, including the role of cytokines in this disease, is under active investigation. The immune system is likely an integral part of normal hair growth and hair growth cycle1 since epidermal keratinocytes, including those of the hair follicle, synthesize a number of cytokines including interleukins, granulocyte colony-stimulating factor, and tumor necrosis factor α (TNF-α).2 These cytokines, however, may also act as mediators of immunity and inflammation and have been implicated in a number of hair diseases including alopecia areata.
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