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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.

Background Severe coronavirus disease-2019 (COVID-19) is associated with dysregulated immune response and extreme inflammatory injury. Considering the role of insulin growth factor-1 (IGF-1) in immune-mediated and inflammatory reactions, this study was conducted to investigate the IGF-1 contribution to the pathogenesis of severe form of COVID-19. Material and methods Sixty-two patients with severe COVID-19 and 52 healthy subjects were enrolled in this study. The serum levels of IGF-1 were measured using a solid-phase enzyme-linked chemiluminescent immunoassay on an Immulite 2000 system (Siemens Healthcare Diagnostics. Result The serum levels of IGF-1 had no significant difference in COVID-19 patients compared to the healthy subjects (p = 0.359). There was a positive correlation between IGF-1 and age in the severe COVID-19 patients, while a negative correlation was observed for the serum levels of IGF-1 and age in the control group (r = 0.364, p = 0.036, r = − 0.536, p = 0.001, respectively). Moreover, IGF-1 was remarkably associated with hypertension, neurogenic disease, shock, and nausea in patients with the severe form of COVID-19 (p = 0.031, p = 0.044, p = 0.01, p = 0.03, respectively). Conclusion Our results pointed to the complex role of IGF-1 in the severe form of COVID-19, and its association with clinical parameters, and some risk factors in the severe form of COVID-19. KeywordsIGF-1 • Severe COVID-19 • Age • Clinical parameters Abbreviations COVID-19 Severe coronavirus disease-2019 IGF-1 Insulin growth factor-1 SARS-CoV-2 Severe acute respiratory syndrome-coronavirus 2 ALI Acute lung injury MOF Multi-organ failure IGF2R Insulin-like growth factor II receptor PI3K/AKT Phosphatidylinositol-3-kinases/protein kinase B MAPK Mitogen-activated protein kinase ARDS Acute respiratory disease syndrome WHO World Health Organization BMI Body mass index BPD Blood pressure diastolic PR Pulse rate RR Respiratory rate Inflammopharmacology Parisa Feizollahi and Somaieh matin contributed equally to this work.

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