Impaired inhibitory function of circulating CD4+CD25+ regulatory T cells in alopecia areata

Alopecia areata (AA) presents as patches of hair loss, and progresses to include the entire scalp (alopecia totalis; AT) or all body regions (alopecia universaris; AU) in 7% of affected individuals. Ophiasis is distinct pattern of AA with extension of alopecia along the scalp margin. These three forms tend to be recalcitrant and have poor prognostic significance. AA is a chronic, organ-specific, and T cell-mediated autoimmune disease affecting the hair follicles. Impaired immune privilege in the hair follicles likely plays a key role in the primary pathogenesis [ 1 Christoph T. Muller-Rover S. Audring H. Tobin D.J. Hermes B. Cotsarelis G. et al. The human hair follicle immune system: cellular composition and immune privilege. Br J Dermatol. 2000; 142: 862-873 Crossref PubMed Scopus (277) Google Scholar , 2 Gilhar A. Paus R. Kalish R.S. Lymphocytes, neuropeptides, and genes involved in alopecia areata. J Clin Invest. 2007; 117: 2019-2027 Crossref PubMed Scopus (222) Google Scholar ]. Loss of immune privilege may be mediated by increased major histocompatibility complex class I under the influence of interferon-gamma, neuropeptides, and immunogenetics, and insufficient activity of regulatory T (Treg) cells [ 2 Gilhar A. Paus R. Kalish R.S. Lymphocytes, neuropeptides, and genes involved in alopecia areata. J Clin Invest. 2007; 117: 2019-2027 Crossref PubMed Scopus (222) Google Scholar , 3 Ito T. Ito N. Bettermann A. Tokura Y. Takigawa M. Paus R. Collapse and restoration of MHC class-I-dependent immune privilege: exploiting the human hair follicle as a model. Am J Pathol. 2004; 164: 623-634 Abstract Full Text Full Text PDF PubMed Scopus (195) Google Scholar ].