Sengul Aksakal; Selim Gorgun
Abstract
Background: The development of a cytokine storm in Coronavirus Disease 2019 (COVID-19) infection can make the disease fatal. We hypothesize that this excessive cytokine production impairs mucosal healing. IL-17 and IL-22 are cytokines that play a key role in protecting and regenerating mucosal tissues. ...
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Background: The development of a cytokine storm in Coronavirus Disease 2019 (COVID-19) infection can make the disease fatal. We hypothesize that this excessive cytokine production impairs mucosal healing. IL-17 and IL-22 are cytokines that play a key role in protecting and regenerating mucosal tissues. IL-17 and IL-22 support each other, and the imbalance between them plays a role in the pathogenesis of many rheumatologic diseases.Objective: To investigate whether COVID-19 severity is related to IL17, IL-22, and the IL-17/IL-22 ratio.Methods: The study was planned prospectively and included 69 patients with active COVID-19 infection. Three groups were created: patients with upper respiratory tract infection, pneumonia, and cytokine storm. Blood samples were taken from the patients upon their first admission and serum levels of IL-17 and IL-22 were measured using the enzyme-linked immunosorbent assay (ELISA). We assessed the relationship between IL17, IL22, IL17/ IL22 ratio, clinical and lung involvement by comparing them with the healthy group.Results: The levels of IL-17 were significantly higher in COVID-19 patients with upper respiratory tract infection compared to the control group (p=0.027). IL17/IL-22 ratio significantly increased in patients with cytokine storm compared to the healthy controls (p=0.027). Serum levels of IL-22 were negatively correlated with the CO-RADS score (r=-0.31, p=0.004), while IL-17/IL-22 ratio was positively correlated with the CO-RADS score (r=0.29, p=0.008). Conclusion: Levels of IL-17, IL-22, and IL-17/IL-22 may provide valuable insights into the progression of COVID-19.
Xiaoqiang Wang; Yang Shen; Xia Ke; Suling Hong
Abstract
Background: T-helper 17 (Th17) cell response is engaged in the onset of allergic rhinitis (AR). Moreover, interleukin (IL)-38 is thought to be involved in inhibiting cytokine secretion in the Th17 pathway.Objective: To evaluate the regulatory function of IL-38 on abnormal Th17 responses in Chinese patients ...
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Background: T-helper 17 (Th17) cell response is engaged in the onset of allergic rhinitis (AR). Moreover, interleukin (IL)-38 is thought to be involved in inhibiting cytokine secretion in the Th17 pathway.Objective: To evaluate the regulatory function of IL-38 on abnormal Th17 responses in Chinese patients with AR.Methods: Forty-five participants, divided into an AR group (n=25) and a control group (n=20), were recruited for the study. In addition, the expression of IL-38 and Th17-related cytokines was measured as well as the Th17 cell count in participants. By implementing recombinant IL-38 (rIL-38), the intervention of human peripheral blood mononuclear cells (PBMCs) was performed. Then, flow cytometry, polymerase chain reaction (PCR), and enzyme-linked immunosorbent assay (ELISA) were used to detect theTh17 milieu.Results: The expression of IL-38 in the AR group notably reduced compared with that in the control, whereas Th17 cell frequency and the expression levels of its transcription factor (RORC) and cytokines (IL-17A and IL-23) increased. The differentiation and immune function of Th17 cells in PBMCs were inhibited by rIL-38.Conclusion: Th17 responses are inhibited by IL-38 in patients with AR. Therefore, the obtained findings indicate that IL-38 is a potential therapeutic target for Chinese patients with AR.
Saeid Abediankenari; Davoud Shaker; Farshideh Abedian; Arazmohammad Mirabi
Abstract
Background: Dendritic cells (DC) are a key regulator of the immune response, and interferon- beta (IFN-β) is considered an immunomodulatory molecule for DC. Objective: The purpose of this study was to evaluate the ability of IFN-β treated DC to induce cytokine secretion by CD4+ T cells. Methods: ...
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Background: Dendritic cells (DC) are a key regulator of the immune response, and interferon- beta (IFN-β) is considered an immunomodulatory molecule for DC. Objective: The purpose of this study was to evaluate the ability of IFN-β treated DC to induce cytokine secretion by CD4+ T cells. Methods: Dendritic cells were generated from blood monocytes with granulocyte-monocyte colony-stimulating factor and interleukin-4 with or without IFN-β. We analyzed the production of CD4+ T helper cytokines (IL-17, IFN- γ and IL-10) in the supernatant of the dendritic cell-T cell co- cultures by ELISA. We also studied the effects of HLA-G and costimulatory molecules on immature and mature DC. Results: IFN-γ and IL-17 decreased significantly in the presence of HLA-Gbearing DC compared to control cultures (p<0.05). Conclusion: Using the mixed leukocyte reaction, we found that DC treated with IFN-β mediated the inhibition of T cell activation via cytokine production. We conclude that this is important for preventing overactivation of the immune system.
