Redox imbalance and IL ‐17 responses in memory CD 4 + T cells from patients with psoriasis

All stages of the inflammatory process involved in T cell‐mediated chronic skin disorders like psoriasis are affected by redox imbalance. On the other hand, Th17 cells have a critical role in the pathogenesis of psoriasis. In this study, we evaluated redox status in memory CD 4 + T cells and plasma of patients with psoriasis and its correlation with IL ‐17 response. To this end, memory T cells were isolated from 10 patients with psoriasis and 10 controls. Intracellular Glutathione ( GSH ), reactive oxygen species ( ROS ) and superoxide as well as IL ‐17 were measured using flow cytometry. Plasma total anti‐oxidant capacity ( TAC ) was quantified by ferric reducing ability of plasma ( FRAP ) assay. The expression of catalase ( CAT ) , superoxide dismutase 1( SOD 1 ), superoxide dismutase 2 ( SOD 2 ), nuclear factor, erythroid 2 like 2 ( NFE 2L2 ) and cytochrome b‐245 beta chain ( CYBB ) genes were analysed using real‐time PCR . Our results showed an increased intracellular ROS production in memory CD 4 + T cells of patients compared to controls , ( P = 0.04). Furthermore, a significant decrease in expression of catalase gene was found in patients, ( P = 0.02). However, no significant differences were observed for intracellular GSH , IL ‐17 and TAC levels between patients and controls. Also, no correlation was seen between the intracellular IL ‐17 level and intracellular ROS , GSH and catalase gene expression levels. Collectively, we found an increased ROS production in stimulated memory T cells of patients that could be due to reduced expression of catalase gene. However, it seems that these redox abnormalities have no relationship with IL ‐17 response in memory T cells.