الفهرس 
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Abstract
Alopecia areata is a medical condition which can affect men women and children. It often appears as well – defined circular bald patches on the scalp. Many people will get just one or two patches, but for some the hair loss can be extensive. Unfortunately, children who develop AA before puberty are most likely to develop more extensive and persistent hair loss.
Hair loss that spreads to cover the entire scalp is called Alopecia totalis, If it spread to over the entire body, affecting scalp eyebrows, lashes, beard, pubic hair and every thing else, then the condition is called alopecia universalis. If the alopecia is just limited to the beard in men, it is called alopecia barbae.
Although there are several hypothesis proposed the etiology of AA, many factors have been described such as genetic susceptibility the atopic state, non specific autoimmune reactions, neurological factors, infectious agents and possible emotional stress.
Current concepts of AA pathogenesis suggest that AA is a nonscarring inflammatory, cell-mediated disease. A perifollicular and intrafollicular mononuclear cell infiltrate of primarily CD4+ and CD8+ cells is closely associated with dystrophic anagen stage HF which suggests that T cells and cytokines play an important role. On the other hand, AA is frequently associted with atopic diseases and anti-nuclear antibodies are frequently found in sera from patients with AA, suggesting that B cells are also activated and involved.
Collectively, multiple and complex immune dysregulations are likely to contribute to the development of the disease.
Induction of IgE synthesis in human B cells requires three types of signals. The first signal is delivered through the B cell antigen receptor, and the second signal is mediated by Th2 cytokines.