الفهرس | Only 14 pages are availabe for public view |
Abstract Alopecia areata (AA) is a common, clinically heterogenous, immune-mediated, non-scarring hair loss disorder. The disease may be limited to one or more discrete, well-circumscribed round or oval patches of hair loss on the scalp or body, or it may affect the entire scalp (alopecia totalis) or the entire body (alopecia universalis). Alopecia areata (AA) is an organ-specific autoimmune disease against hair follicles (HFs). Anagen HFs are immunopurified sites with down-regulation of major histocompatibility complex (MHC) class I antigens as well as with local expression of potent immunoinhibitory signaling milieu and are escaping from attacks by cytotoxic T cells (CTLs). HFs also appear to down-regulate the expression of ligands that stimulate the activation of natural killer (NK) cells, which are primed to recognize and eliminate MHC class I negative cells. A collapse of the immunoprivilege and subsequent cell-mediated cytotoxicity to HFs has been considered essential to the pathogenesis of AA. Accordingly, it has been reported that CD4+ T cells, CD8+ T cells, and NK cells, but not basophils, prominently infiltrate around anagen HFs in active AA lesions. It has been revealed that granulysin is a cytolytic granule protein that acts synergistically with perforin and induces apoptosis of human cells. Activated CTLs and NK cells express granulysin, and the serum concentration of granulysin is considered to reflect the activity of these cells. Granulysin is steady in the serum and its half-life is longer than that of cytokines, therefore evaluation of serum granulysin levels is useful for monitoring cell-mediated cytotoxic immune responses in vivo. The aim of the current study was to study whether granulysin level, which is known to reflect the activity of cytotoxic immune response, is related to the disease activity of alopecia areata. |