Autoantibodies (AABs) play a critical role in the pathogenesis of autoimmune diseases (AIDs) and serve as a diagnostic and prognostic tool in assessing these complex disorders. Viral infections have long been recognized as a principal environmental factor affecting the production of AABs and the development of autoimmunity. COVID‐19 has primarily been considered a hyperinflammatory syndrome triggered by a cytokine storm. In the following, the role of maladaptive B cell response and AABs became more apparent in COVID‐19 pathogenesis. The current review will primarily focus on the role of extrafollicular B cell response, Toll‐like receptor‐7 (TLR‐7) activation, and neutrophil extracellular traps (NETs) formation in the development of AABs following SARS‐CoV‐2 infection. In the following, this review will clarify how these AABs dysregulate immune response to SARS‐CoV‐2 by disrupting cytokine function and triggering neutrophil hyper‐reactivity. Finally, the pathologic effects of these AABs will be further described in COVID‐19 associate clinical manifestations, including venous and arterial thrombosis, a multisystem inflammatory syndrome in children (MIS‐C), acute respiratory distress syndrome (ARDS), and recently described post‐acute sequelae of COVID‐19 (PASC) or long‐COVID.

The dysregulated immune response is one of the cardinal features of severe coronavirus disease-2019 (COVID-19). This study has been conducted to clarify the occurrence of AABs associated with a systemic autoimmune rheumatic disease (SARD) in hospitalized patients with a moderate, severe, and critical form of COVID-19. The serum samples obtained from one hundred seventy-six hospitalized COVID-19 patients were enrolled in this study, including patients with moderate (N = 90), severe (N = 50), and critical (N = 36) forms of COVID-19. Serum samples collected from healthy subjects before the COVID-19 pandemic were used as control. The ANA, ds-DNA, c-ANCA, p-ANCA, aPL, and anti-CCP occurrence was evaluated using a solid-phase enzyme-linked immunosorbent assay (ELISA). The occurrence of ANA, anti-dsDNA, Anti-CCP, c-ANCA, and p-ANCA was significantly higher in the COVID-19 patients compared to serum obtained from healthy subjects (P = 0.0001, P = 0.0001, P = 0.0001, P = 0.030, and P = 0.001 respectively). The positive number of anti-CCP tests increased significantly in severe COVID-19 compared to the moderate group (P = 0.002). Our study further supports the development of autoantibodies related to systemic autoimmune rheumatologic diseases (SARD). To the best of our knowledge, this is the first study with a large sample size that reported the occurrence of anti-CCP in a severe form of COVID-19.

Background Cardiovascular disease (CVD) is the most common cause of mortality in rheumatoid arthritis (RA), and Inflammation has a decisive role in its pathogenesis. CXCL9 contributes to multi aspects of inflammatory reactions associated with the pathogenesis of CVD. In the current study, we evaluated the association of plasma CXCL9 and CXCR3 gene expression with Cardiovascular risk factors in RA patients for the first time.Material and methods Thirty newly diagnosed, 30 under-treatment RA patients and 30 healthy subjects were recruited in this study. The plasma concentration of CXCL9 and CXCR3 gene expression were measured using ELISA and Real-Time PCR, respectively. The CVD risk was evaluated using Framingham Risk Score (FRS) and Systematic Coronary Risk Evaluation (SCORE).Results The plasma levels of CXCL9 were significantly higher in the newly diagnosed and under-treatment RA patients compared to the control group (P < 0.0001 and P < 0.001, respectively). Also, The CXCR3 gene expression was remarkably elevated in newly diagnosed and under-treatment patients (P < 0.001 and P < 0.01, respectively). The CXCL9 and CXCR3 were remarkably associated with RA disease activity (P = 0.0005, r = 0.436; P = 0.0002, r = 0.463, respectively). The FRS was remarkably higher in newly diagnosed and under-treatment patients (P = 0.014 and P = 0.035, respectively). The CXCR3 gene expression significantly correlated with age, systolic blood pressure, FRS, and SCORE (P = 0.020, r = 0.298; P = 0.006, r = 0.346; P = 0.006, r = 0.349; P = 0.007, r = 0.341, respectively). The CXCL9 plasma concentration had a significant negative correlation with plasma HDL and LDL levels (P = 0.033, r=-0.275; P = 0.021, r=-0.296, respectively).Conclusion CXCL9 and CXCR3 correlates with different variables of CVD in RA.