Abstract

Cytokines have long been postulated to play a role in alopecia areata (AA), and antigen-specific scalp T cells from patients with extensive AA have been found to have an intrinsic defect in the production of TH1 cytokines such as interferon gamma and interleukin 2 (IL-2).1,2 In the interesting study presented by Castela et al,3 5 patients with extensive AA were treated with low-dose IL-2, and 4 of the 5 patients attained considerable hair regrowth. This was accompanied by an increase in regulatory T (Treg) cells; cells defined by the expression of CD4, CD25, and transcription factor forkhead box P3 (FOXP3) in skin biopsy specimens; and no significant change in circulating Treg cells. Adverse effects in this study were reported to be minimal. The investigators in the Department of Dermatology at University Hospital in Nice, France, continue to enroll research participants and list this study as a clinical trial on ClinicalTrials.gov (NCT01840046). Dysfunctional Treg cells have been identified and characterized in autoimmune diseases, such as psoriasis, multiple sclerosis, and autoimmune polyglandular syndrome type 1, suggesting that normal Treg function is important to the prevention of autoimmune disease. In the mouse model for AA, the C3H/HeJ mouse, a low level of skin CD4+CD25+ Treg cells has been found in the skin, and in this same model, injection of CD4+CD25+Treg cells was found to prevent the induction of AA by CD4+CD25– T cells as well as CD8+ T-cell–induced localized hair loss.4-6

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