Abstract
Recent clinical and experimental studies have provided insights into the pathological mechanisms of alopecia areata and revealed that it is an organ-specific and cell-mediated autoimmune disease. Various triggers, such as viral infections, trauma, hormones, and emotional/physical stressors, can activate autoreactive cytotoxic T cells（CTL）, which produce interferon（IFN）-γ. IFN-γ abrogates the immune privilege of hair follicles（HF）, upregulates CXCL10 expression, and induces higher interleukin 15 expression in HF keratinocytes. HF autoantigens are subsequently recognized by CTL, which results in hair loss. During these immunological responses, cytokines and chemokines are regarded as key players that mediate autoimmune inflammation. Interestingly, JAK inhibitors have been found to produce dramatic improvements in alopecia areata in both humans and C3H/HeJ mice. This review suggests that therapies that target cytokines/chemokines could be useful for alopecia areata.
