Department of Dermatology, University of California, San Francisco, California, USA

Correspondence: Vera H. Price, Department of Dermatology, University of California, San Francisco, 350 Parnassus Avenue, Suite 404, San Francisco, CA 94117, USA. Email: vhprice@orca.ucsf.edu

Received 30 December 2002; Accepted 13 February 2003.

Abstract

Over the past decade, basic research has established alopecia areata as a T cell–mediated autoimmune disease and has clarified many of its genetic, cellular, and molecular aspects. Perifollicular and intrafollicular mononuclear cell infiltrates directed at anagen hair bulbs are characteristic and striking histologic features in early alopecia areata. The inflammatory infiltrate is composed predominantly of activated CD4+and CD8+T cells, together with macrophages and Langerhans cells. The initiation phase of alopecia areata is mediated by type 1 cytokines, including interleukin-2, interferon-, and tumor necrosis factor-. Like other diseases with a strong autoimmune component, alopecia areata has associated with it specific human leukocyte antigens, which determine susceptibility, severity, chronicity, and resistance. New topical immunomodulating drugs and biologic therapies that have been developed, or that are in development, for the treatment of other immune-mediated inflammatory skin diseases will likely be effective in alopecia areata as well. The present discussion addresses the treatment of alopecia areata within the framework of these new modalities.