@article { author = {Mohammadi, Saeed and Sedighi, Sima and Memarian, Ali}, title = {IL-17 is Aberrantly Overexpressed Among Under-treatment Systemic Lupus Erythematosus Patients}, journal = {Iranian Journal of Pathology}, volume = {14}, number = {3}, pages = {236-242}, year = {2019}, publisher = {Farname Inc in collaboration with Iranian Society of Pathology}, issn = {1735-5303}, eissn = {2345-3656}, doi = {10.30699/ijp.2019.94878.1934}, abstract = {Background & Objective: Systemic lupus erythematosus (SLE) is an autoimmune disease with chronic inflammatory immune response. Current therapies mostly rely on glucocorticoids which are accompanied by side-effects and mostly fail to achieve a favorable remission. Th17 subpopulation of T cells is increased in exacerbated SLE as IL-17 cytokine is overexpressed. However, IL-17 is reported to be resistant to glucocorticoids in various disorders. Here, we evaluated the plasma level of IL-17 among newly diagnosed and under-treatment SLE patients to understand the effect of glucocorticoids on Th17 response.  Methods: A total of 40 female SLE patients and 20 age- and sex- matched normal subjects were enrolled. IL-17 plasma level was evaluated using ELISA cytokine assay and analyzed with previously obtained IL-10, IFN-γ, and GILZ levels. Results: Our findings revealed that IL-17 was overexpressed among under-treatment SLE patients. There was a significant correlation between IL-17 and IFN-γ and significant reverse correlations between IL-17, IL-10, and GILZ levels. IL-17 was not significantly correlated with the disease activity. Conclusion: According to the role of IL-17 in tissue injury and the fact that glucocorticoids are not successful in preventing organ damages in SLE, the overexpressed IL-17 in response to therapies could be introduced as an underlying reason.}, keywords = {Systemic Lupus Erythematosus,IL-17,glucocorticoids,pathogenesis,organ damage,Treatment}, url = {https://ijp.iranpath.org/article_36276.html}, eprint = {https://ijp.iranpath.org/article_36276_1a583426f906145563c1ac18d3587060.pdf} }