Abstract
Background Psoriasis is a Th1/Th17 disease resulting from a dysregulated interplay between keratinocytes and immune cells, leading to skin hyperproliferation. Increased levels of interleukin (IL)-33 were reported in various Th1/Th17-driven autoimmune diseases, such as rheumatoid arthritis and inflammatory bowel disease, with correlation to disease severity. Increased levels of IL-33 have been reported in lesional skin of psoriatic patients. The authors hypothesized that keratinocyte-released IL-33 might play a role in psoriasis pathogenesis; thus, inhibiting IL-33 activity might be a breaking new therapeutic strategy in its treatment. Patients and methods Serum IL-33 levels were measured by an enzyme-linked immunosorbent assay for 30 patients with active psoriasis (group A), 30 patient with stable psoriasis (group B), and 30 healthy age-matched and sex-matched controls (group C). Results Serum IL-33 showed statistically significant higher mean value among patients with psoriasis compared with the control group. The level of IL-33 in active psoriasis was significantly higher than in inactive psoriasis. Moreover, there was a statistically significant correlation between IL-33 and psoriasis area and severity index (PASI) score. Receiver operating characteristics curve detected the validity of serum IL-33 in differentiating patients with psoriasis from controls. At the cutoff point of IL-33 as 22.72 pg//ml, psoriasis could be predicted with 96.67% sensitivity and 93.33% specificity. Serum IL-33 was a statistically significant predictor of PASI score, with 63.5% of PASI scores predicted by serum IL-33. Conclusion Serum IL-33 may represent a new marker for psoriasis diagnosis as well as a predictor of the disease severity.
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