¹Department of Dermatology, Richard and Adeline Fleischaker Chair in Dermatology Research, University of Oklahoma Health Sciences Center, Adjunct Investigator, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma, USA

Correspondence: Dr Richard D. Sontheimer, Department of Dermatology, University of Oklahoma Health Sciences Center, 619 NE, 13th Street, Oklahoma City, Oklahoma 73104, USA. E-mail: richard-sontheimer@ouhsc.edu

Received 8 February 2008; Revised 27 March 2008; Accepted 14 April 2008; Published online 26 February 2009.

Abstract

A number of uncommon, clinically diverse and poorly understood inflammatory skin diseases are linked by the presence of a set of histopathological elements that have traditionally been referred to as the "lichenoid tissue reaction/interface dermatitis" (LTR/IFD). The prototypic skin disease in this category is lichen planus. However, the LTR/IFD can also be seen in skin disorders associated with systemic illnesses (lupus erythematosus, dermatomyositis), and the skin changes of potentially fatal disorders such as graft-versus-host disease, Stevens–Johnson syndrome, and toxic epidermal necrolysis. It has been traditionally felt that cytotoxic T-lymphocytes represent the final effector cell type for the epidermal basal cell layer injury pattern that is common to LTR/IFD disorders. Recent work has suggested that a number of different LTR/IFD skin disorders share a common inflammatory signaling pathway involving the actions of plasmacytoid dendritic cell-derived IFN-. This signaling pathway appears to amplify cytotoxic T cell injury to the epidermal basal cell compartment. This review will summarize the work implicating this pathway as well as the other cellular and molecular mechanisms that are thought to be responsible for the prototypic LTR/IFD disorder, lichen planus. It is hoped that a better understanding of the immunological commonalities shared by various LTR/IFD disorders will lead to more effective safer treatment options for these illnesses.