Certain Cytokines Play Role in Cutaneous Lupus Erythematosus Development, According to Study
Recent research highlights the understudied role of cytokines in various subtypes of cutaneous lupus erythematosus, primarily that cytokines interleukin-1 (IL-1-beta), interleukin-17 (IL-17) and tumor necrosis factor-alpha (TNF-alpha) are involved in the pathogenesis of the disease. These results were recently presented at the 74th Annual Meeting of the American Academy of Dermatology March 4-8 in Washington, D.C.
Lupus is an autoimmune disease that affects multiple organs and systems in the body. When autoimmunity is specific to the skin, the disease is termed cutaneous lupus and this, according to the American Skin Association, can be divided in three main categories: chronic cutaneous lupus (CCLE), subacute cutaneous lupus (SCLE) and acute cutaneous lupus (ACLE).
In addition, CCLE can be further broken down into discoid lupus (DLE), its most common form, due to the coin-like shape of its skin lesions.
Cytokines, small proteins essential in cell signaling, play a role in inflammation and autoimmunity, and have largely been studied in lupus in the context of the pathogenesis of the systemic form of the disease. However, the role of cytokines in the etiology and inflammation exacerbations in cutaneous lupus erythematosus has not been thoroughly investigated.
Researchers analyzed skin samples from 59 patients with subacute lupus erythematosus (17 patients), discoid LE (21 patients), and LE tumidus (17 patients), a rare type of lupus characterized by edematous erythematous plaques.
American College of Rheumatology (ACR) criteria for systemic lupus erythematosus (SLE) was met by 70.5 percent of subacute LE patients, by 19 percent of discoid patients, and by 19 percent of tumidus LE patients. Through immunohistochemical assays, researchers assessed the presence of interleukin (IL)-1-beta, IL-17, IL-18, IL-10, IL-6, and tumor necrosis factor-alpha (TNF-a).
Results showed that, when compared to discoid and tumidus subtypes, patients with subacute LE had increased levels of IL-1-beta, IL-18 and TNF-a. On the other hand, epidermal IL-17 was higher in patients with CLE and SLE, while dermal expression was lower. Moreover, patients with CLE and SLE had lower expression of IL-17 and higher expression of IL-1. Expression of TNF-a and IL-1 correlated in patients with discoid and tumidus subtypes of LE, with no differences observed in the immunoexpression of IL-10 or IL-6.
These findings add to the theory that different cytokines play various roles in different subtypes of lupus and that further research is needed.