الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
Alopecia areata (AA) is an autoimmune disease of the hair follicle, resulting in acute or chronic patches of non-scarring hair loss, total hair loss of the scalp (alopecia totalis, AT), or complete hair loss of entire body and scalp (alopecia universalis, AU). It is a disease with significant impact on health-related quality of life.
Alopecia areata (AA) is hypothesized to be an organ-specific autoimmune disease, mediated by T lymphocytes, resulting from disturbances in hair follicle immune privilege with genetic predisposition and an environmental trigger that targets anagen hair follicles.
The concept of autoimmunity in AA is supported by the high rate of association with other immune-mediated diseases like thyroid disease, Vitiligo and Systemic lupus erythematosus .
The role of ESRβ on the pathogenesis of AA has not been studied yet. ERβ is the major steroid receptor expressed in both male and female human non-balding scalp hair follicles. In human occipital scalp hair follicles, E2 inhibits hair shaft elongation in both males and females invitro. However, hair shaft elongation in human frontotemporal anagen hair follicles was inhibited in females and stimulated in males.