Macrophage polarization induced immune dysregulation in rheumatoid arthritis

Abstract

Background and objective: Rheumatoid arthritis (RA) is one of the most prominent inflammatory autoimmune illnesses, causing polyarticular synovitis. The precise causes of RA are still unknown; however, chronic inflammation patterns are influenced by a combination of immunological, environmental, and epigenetic factors. Anti-CCP antibodies are a particular biomarker for RA diagnosis and severity. Alterations of complement components and pro- and anti-inflammatory cytokines are critical to the pathogenesis of RA. The current study intended to compare and examine the immunological properties of anti-CCP, IL-10, IL-17, and C5a antibodies in samples from RA patients and healthy individuals. The study evaluated medication exposure and various immune markers simultaneously to enhance immunological profiling, clinical accuracy, and classification of patients with RA Methods: The Cobas e 411 analyzer was used to measure the anti-CCP antibody levels in the serum of 60 RA patients and 40 healthy individuals. Enzyme-linked immunosorbent assay (ELISA) technique from the BioTek ELx800 was used to estimate the levels of IL-17, IL-10, and C5a in the sera of participants. Both groups were matched in age and ethnicity. An unpaired T-test was used to analyze data statistically using the GraphPad Prism 8 program. The ANOVA test was used for more than 2 groups. Results: The current study indicated that patients with rheumatoid arthritis (RA) had a significantly lower concentration of IL-10 serum levels as compared to the healthy controls, yet with increased levels of IL-17, C5a, and anti-CCP antibodies. Some of the causes of the decrease in IL-10 might be chronic inflammation and the suppressive action of the pro-inflammatory cytokines on its production and signaling. Further, RA patients under corticosteroid treatment had reduced levels of IL-17, C5a, and anti-CCP antibodies compared to untreated patients, showing corticosteroid therapy lowers the inflammatory mediators without restoring the IL-10 levels. Conclusion: It can be concluded that macrophages from rheumatoid arthritis patients shifted from anti-inflammatory (like IL-10) to pro-inflammatory (like IL-17) properties. Patients with rheumatoid arthritis had lower levels of anti-inflammatory cytokine markers like IL-10 and greater levels of pro-inflammatory cytokines like IL-17, inflammatory markers like C5a, and rheumatoid arthritis markers like anti-CCP.