A hallmark of COVID-19 is the variety of complications that follow SARS-CoV-2 infection in some patients, and that target multiple organs and tissues. Also remarkable are the associations with several auto-inflammatory disorders and the presence of autoantibodies directed to a vast array of antigens. The processes underlying autoantibody production in COVID-19 have not been completed deciphered. Here, we review mechanisms involved in autoantibody production in COVID-19, multisystem inflammatory syndrome in children, and post-acute sequelae of COVID19. We critically discuss how genomic integrity, loss of B cell tolerance to self, superantigen effects of the virus, and extrafollicular B cell activation could underly autoantibody proaction in COVID-19. We also offer models that may account for the pathogenic roles of autoantibodies in the promotion of inflammatory cascades, thromboembolic phenomena, and endothelial and vascular deregulations.
Keyphrases
- coronavirus disease
- sars cov
- respiratory syndrome coronavirus
- systemic lupus erythematosus
- oxidative stress
- gene expression
- end stage renal disease
- intensive care unit
- newly diagnosed
- ejection fraction
- immune response
- endothelial cells
- high resolution
- peritoneal dialysis
- dendritic cells
- atrial fibrillation
- mass spectrometry
- risk factors
- drug induced
- extracorporeal membrane oxygenation