Rethinking the Pathogenesis of Cutaneous Lupus

Knowledge of the etiology of cutaneous lupus is rapidly evolving. Dissection of the pathologic events in lesional skin has led to knowledge of important cell populations and transcriptional changes contributing to disease. Recently, the study of nonlesional skin in patients with systemic lupus has also identified key abnormalities that likely contribute to a propensity for inflammation. These include an elevated type I IFN signature, overproduction of IFNs, and an absence of Langerhans cells. These changes promote aberrant inflammation in response to known triggers of disease, such as UV light. Further research will undoubtedly accelerate our understanding of this disfiguring disease.

Automated summary

Recent research on cutaneous lupus has identified key abnormalities in nonlesional skin of patients with systemic lupus, including an elevated type I interferon signature, overproduction of interferons, and absence of Langerhans cells. These abnormalities likely contribute to a propensity for inflammation in response to disease triggers like UV light.