Alopecia areata pathogenesis is primarily influenced by interleukin 15 produced by hair follicles in response to T-cell–secreted interferon-γ. This process is mediated by Janus kinase (JAK) 1/2 and JAK 1/3 signaling in T cells, which respond to hair follicle–derived interleukin 15 with more interferon-γ production, thus creating a positive pathologic feedback loop. Accordingly, pharmacologic inhibitors of the JAK signaling pathway have emerged as highly effective treatment options for alopecia areata patients. Disease resolution, either spontaneously or after treatment with a JAK inhibitor, results in the reentry of hair follicles into the anagen state and rapid hair growth. Central centrifugal cicatricial alopecia (CCCA) is a progressive scarring alopecia predominately occurring in women of African descent.¹ The progression of hair loss is insidious, often occurring in the absence of clinical signs of overt inflammation. As a result, end stage fibrosis occurs at a rate disproportionate to the rate of inflammation, a finding common to a class of disorders termed fibroproliferative disorders (FPDs).

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Sandra Jones

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Hair Therapy and Transplantation

Email: hairtherapy@emedscholar.com