Interferon-gamma in patients with alopecia universalis
Alopecia areata (AA) is a non-scarring inflammatory disease of the hair follicle. Although it usually presents as asymptomatic localized hair loss, it is a disese of very broad spectrum. Alopecia universalis (AU) is an uncommon form of AA that involves the loss of all haed and body hair and is estimated to account approximately 5% of all alopecia cases [1]. The cause of disease is unknown, although there is evidence to suggest that the link between lymphocytic infiltration of the follicle and the disruption of the hair follicle cycle in AA may be provided by a combination of factors, including cytokine release, cytotoxic T-cell activity, and apoptosis [2,3]. It is also considered that a disequilibrium in the production of cytokines, with a relative excess of proinflammatory and Th1 types, vs. anti-inflammatory cytokines may be involved in the persistence of AA lesions, as shown in human scalp biopsies [4]. The immune response presented in AU is associated with aberrant lesional expression of interferon-gamma (IFN-γ), interleukin-2 (IL-2) and IL-1β, and overexpression of ICAM-1 and MHC molecules on hair follicle keratinocytes and dermal papilla cells [5].