Epidemiologic and genetic characteristics of alopecia areata (part 1)

Abstract

Alopecia areata (AA) is a common, chronic, inflammatory disease resulting in an unpredictable, non-scarring form of hair loss. It affects almost 0.1% of the general population. Although the cause of AA is poorly understood, it is hypothesized to have an autoimmune etiology. Supporting this theory is the fact that activated CD4 and CD8 T lymphocytes have been found in characteristic perifollicular and intrafollicular inflammatory infiltrates of affected individuals' anagen hair follicles. AA provides an excellent opportunity to study the role of immunogenetics. In fact, various genes that have a role in regulating immunity have also been associated with susceptibility to AA. Several reports have indicated a significant association between AA and certain human leukocyte antigens (HLA) genes such as HLA-DRB1*0401 and DQB1*. This review provides an overview of current knowledge about the molecular genetics of AA. The literature review has shown overlapping gene patterns suggestive of common pathogenic mechanisms. However, many questions remain unanswered because data about local gene expression patterns in affected tissues are still scarce.