Details

Autor(en) / Beteiligte

• Esmaeili, Behnaz
• Mansouri, Parvin
• Doustimotlagh, Amir Hossein
• Izad, Maryam

Titel

Redox imbalance and IL‐17 responses in memory CD4+ T cells from patients with psoriasis

Ist Teil von

• Scandinavian journal of immunology, 2019-01, Vol.89 (1), p.e12730-n/a

Ort / Verlag

England: Wiley Subscription Services, Inc

Erscheinungsjahr

2019

Quelle

Wiley-Blackwell Journals

Beschreibungen/Notizen

• 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 CD4 + 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(SOD1), superoxide dismutase 2 (SOD2), nuclear factor, erythroid 2 like 2 (NFE2L2) and cytochrome b‐245 beta chain (CYBB) genes were analysed using real‐time PCR. Our results showed an increased intracellular ROS production in memory CD4 + 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.