Molecular consideration relevant to the mechanism of the comorbidity between psoriasis and systemic lupus erythematosus (Review).

Abstract

Systemic lupus erythematosus (SLE), a common autoimmune disease with a global incidence and newly diagnosed population estimated at 5.14 (range, 1.4-15.13) per 100,000 person-years and 0.40 million people annually, respectively, affects multiple tissues and organs; for example, skin, blood system, heart and kidneys. Accumulating data has also demonstrated that psoriasis (PS) can be a systemic inflammatory disease, which can affect organs other than the skin and occur alongside other autoimmune diseases, such as inflammatory bowel disease, multiple sclerosis, rheumatoid arthritis and SLE. The current explanations for the possible comorbidity of PS and SLE include: i) The two diseases share susceptible gene loci; ii) they share a common IL-23/T helper 17 (Th17) axis inflammatory pathway; and iii) the immunopathogenesis of the two conditions is a consequence of the interactions between IL-17 cytokines with effector Th17 cells, T regulatory cells, as well as B cells. In addition, the therapeutic efficacy of IL-17 or TNF-α inhibitors has been demonstrated in PS, and has also become evident in SLE. However, the mechanisms have not been investigated. To the best of our knowledge, there remains a lack of substantial studies on the correlation between PS and SLE. In the present review, the literature, with regards to the epidemiology, genetic predisposition, inflammatory mechanisms and treatment of the patients with both PS and SLE, has been reviewed. Further investigations into the molecular pathogenic mechanism may provide drug targets that could benefit the patients with concomitant PS and SLE.