Correlation between IL-17, TGF-β and PTPN-22 Levels and Covid-19 Severity in Patients with and without Autoimmune Diseases

Document Type : New and original researches in the field of Microbiology.

Authors

1 Department of Microbiology, Faculty of Pharmacy, Assiut University

2 Department of Microbiology, Faculty of Medicine, Assiut University

Abstract

Background: The Coronavirus pandemic is the most significant global health crisis of our era. Since it first appeared in late 2019, the virus has spread to every continent. Furthermore, systemic inflammation is a common feature in many autoimmune diseases, increasing the risk of cardiovascular and thromboembolic diseases, which have also been linked to COVID-19. Objectives: This study aimed to identify the expression of IL-17 and TGF-β as predictors of COVID-19 severity in patients with and without autoimmune disease. Additionally, the study sought to investigate the role of protein tyrosine phosphatase non-receptor type 22 (PTPN-22) in the progression of COVID-19 in patients with autoimmune disease. Methodology: The study involved 52 COVID-19 patients, 26 having autoimmune disease and 26 not having any known autoimmune disease, along with 26 healthy controls. The expression levels of Il-17, TGF-β, and PTPN-22 were determined using the qRT-PCR technique. Data was collected and analyzed using SPSS. Results: Levels of IL-17 and PTPN-22 were significantly elevated in non-autoimmune COVID-19 patients, while TGF-β levels were significantly higher in the autoimmune group. Furthermore, all markers showed significant correlations with various laboratory biomarkers in both groups. Conclusion: The study found that IL-17 and PTPN-22 were significantly upregulated in patients without autoimmune inflammatory diseases (AID), with IL-17 showing strong correlations with inflammation and coagulation markers. Pro-inflammatory cytokines, including IL17A, were found to have the strongest association with COVID, and their levels may serve as potential risk factors for the severe progression of COVID to acute respiratory distress syndrome (ARDS).

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