Autoantibodies May Underpin Clotting Effects of COVID-19!
Circulating antiphospholipid autoantibodies may contribute to endothelial cell activation and dysfunction in severe COVID-19. In 2020, the same researchers reported results from a preclinical study demonstrating that autoantibodies from patients with active COVID-19 caused clotting in mice. While endothelial dysfunction has been implicated in the widespread thrombo-inflammatory complications of COVID-19, the upstream mediators of endotheliopathy remain for the most part cryptic.
@hillol The presence of circulating antiphospholipid antibodies was a strong marker of the ability of COVID-19 serum to activate endothelium. Further analyses revealed that for a subset of serum samples from patients with severe infection, this activation could be mitigated by depleting total immunoglobulin G (IgG). On the basis of these results, the researchers hypothesize that antiphospholipid autoantibodies may characterize antibody profiles in severe COVID-19 that activate the endothelium and transition the usually quiescent blood-vessel wall interface toward inflammation and coagulation.