Cutaneous lupus erythematosus: molecular and cellular basis of clinical findings.

Abstract

Cutaneous lupus erythematosus (CLE) is a heterogeneous autoimmune disease with welldefined skin lesions, including acute CLE, subacute CLE, chronic CLE and intermittent CLE. In the first part of the review, we discuss the variable relationships that exist between the different clinical forms of CLE and the risk of systemic disease activity. Furthermore, we focus on the annular and papulosquamous forms of subacute CLE and emphasize dermal scarring as a characteristic feature of chronic discoid skin disease in contrast to other subtypes of CLE. Various environmental factors influence the clinical expression of CLE and a striking relationship has emerged between sunlight exposure and the various subtypes of this disease. In the second part, we review the evidence for the abnormal long-lasting photoreactivity in CLE, with an overview of the molecular and cellular factors that may underlie this abnormality. In particular, we discuss the role of UV-mediated induction of apoptosis, mediators of inflammation, such as cytokines and chemokines, nitric oxide, T cell-mediated injury, and the influence of regulatory CD4+CD25+ T cells. However, a complete understanding of the diverse pathophysiologic mechanisms and interactions in CLE does not exist and, as there is yet no convincing animal model of CLE, many studies remain descriptive in nature.