Alopecia areata and chemokine

Abstract

Alopecia areata (AA) is a widely prevalent non-scarring hair loss disease. AA typically presents as asymptomatic well-defined round or oval patches of alopecia. Alopecia is classified based on the extent or pattern of the hair loss. Alopecia totalis (AT) is the loss of all hair on the scalp. Alopecia universalis (AU) is a 100% loss of all scalp and body hair. Alopecia ophiasis is the band like hair loss in the parieto-temporo-occipital area. Evidence suggests that AA is the organ-specific autoimmune disease that have certain genetic background. Hitopathologically, a peribulbar mononuclear cell infiltrate (“swarm of bees”) is characteristic in the acute phase, suggesting that chemokines play pivotal roles in the disease manifestation by the recruitment of these cells. In a study examining serum chemokine levels in 85 AA patients including 22 patients with “mono AA” (patients with one or two lesions of AA), 37 patients with “poly AA” (patients with three or more lesions of AA), and 26 patients with “AT/AU” (patients who experienced complete baldness in the past or in the 3-month observation period after taking blood samples), serum IP-10, MCP- 1, MIP-1α and MIP-1β levels were not significantly elevated in patients with AA compared with normal controls, while serum MIG, RANTES, IL-8 and eotaxin levels were significantly increased in patients with AA compared with normal controls. Additonally, serum MIG and RANTES levels were higher when the disease was active. Another study investigated chemokine mRNA expressions in biopsy samples from AA patients using in situ hybridization and demonstrated the strong expression of MIG, a moderate expression of MCP-1 and a weak expression of IP-10. In AA-affected mice, CCL2, CCL5 (RANTES), CXCL10, CCL17 and CCL20 expressions were upregulated in lymph node cells compared with normal mice. Also, CCL2, CCL5 and CCL17 expressions were elevated also in the AA-affected dermis in comparison to normal controls. Collectively, these findings demonstrate the importance of chemokines and their receptors in the pathogenesis of AA and suggest that they may be therapeutic targets in the disease.