Fig. 4

Pathological features shared by COVID-19 and RA: In both diseases there is immense inflammation of structures that form the inner surfaces of the body, and tissue damage and responses that eventually lead to organ failure. In COVID-19, alveolar epithelial cell damage and T cell activation that cause an increase in local production of pro-inflammatory effector cytokines and exaggerated accumulation of neutrophils and macrophages leading to a profound and uncontrolled immune response. Barrier damage, activation of T-cells, production of effector cytokines and neutrophil influx are also pertinent to synovitis, and RA shares some of these mediators with COVID-19. In COVID-19, structural damage and inflammation in COVID-19 largely confined to the lungs, which are destroyed progressively. Furthermore, and most likely due to activation of robust interleukin-6, COVID-19 mounts systemic acute-phase responses, similar to those in RA [81]. (Image created with Biorender.com)