Recently presented research suggests the cytokines interleukin-1, interleukin-17 and tumor necrosis factor-alpha are involved in the pathogenesis of cutaneous lupus erythematosus subtypes at the epidermis and dermis.
Researchers obtained skin samples from 59 patients with subacute lupus erythematosus (LE; n = 17), discoid LE (n = 21) and LE tumidus (n = 17). Overall, 20 patients with cutaneous LE fulfilled American College of Rheumatology (ACR) criteria for systemic LE (SLE). ACR criteria for SLE was met by 70.5% of subacute LE patients, by 19% of discoid patients and by 19% of tumidus LE patients. Skin samples were immunohistochemically targeted with the monoclonal antibodies interleukin (IL)-1-beta, IL-17, IL-18, IL-10, IL-6 and tumor necrosis factor-alpha (TNF-a).
Increased IL-1-beta, IL-18 and TNF-a were found in patients with subacute LE compared to patients with discoid and tumidus subtypes. Epidermal IL-17 was higher in patients with cutaneous LE (CLE) and SLE compared to patients with discoid and tumidus LE, while dermal immunoexpression was lower. Higher expression of IL-1 and lower dermal expression of IL-17 was observed in patients with CLE and SLE. The expression of TNF-a and IL-1 correlated in patients with discoid and tumidus subtypes of LE, while no differences were observed in the immunoexpression of IL-10 or IL-6.
“Most of the current knowledge about cytokines in LE comes from the study of the systemic form,” the researchers wrote. “The role of the cytokines may be different in the various subtypes of cutaneous LE, if associated or not with systemic LE, but there are only few data comparing them to each other.” – by Shirley Pulawski
Fogagnolo L, et al. Paper #3806. Presented at: American Academy of Dermatology 74th Annual Meeting; March 4-8, 2016; Washington, D.C.
Disclosure: Relevant financial disclosures were not available at the time of publication of this article.