In common with a number of inflammatory autoimmune diseases, genetic factors including HLA class II associations have been identified in alopecia areata. No consensus has been reached on the identity of a specific disease target within the hair follicle in alopecia areata. Suggested candidate cell types include the dermal papilla cells, the keratinocytes of the matrix and presumptive cortex and the hair bulb melanocytes, but these need not be mutually exclusive. The pathogenesis is known to involve disturbance of immune function but there is no proof that an autoimmune mechanism is fundamental. We propose a pathogenetic model incorporating polygenic determination of disease susceptibility and severity with additional, possibly environmental, factors as triggers for disease expression.