TO SHOw how we have been ENgaged in the APS FiELD (What we learned on APS collaborating with Professor Yehuda Shoenfeld)

Abstract

The present review reports the history of our scientific collaboration with Professor Shoenfeld's group. The collaboration started at the end of the 80s and was mainly focused on studies on the pathogenetic mechanisms of the anti-phospholipid syndrome (APS). Following the initial collaborative studies on antibodies against endothelium in systemic autoimmune vasculitis, we were able to use a similar strategy in APS. This line of research has resulted in the characterization of beta 2 glycoprotein I (β2GPI)-dependent anti-phospholipid antibodies (aPL) as mechanisms capable of mediating an endothelial perturbation crucial for the pathogenesis of APS. Thanks to these studies, the collaboration has led to the characterization of the membrane receptors for β2GPI and the cellular signaling resulting from antibody binding. This mechanism has also been shown to mediate the aPL effect on other cell types involved in APS pathogenesis. Finally, the exchange of information made it possible to replicate and extend the setting of animal models of the syndrome, which proved to be valuable tools for understanding the pathogenesis of the syndrome. It has been a long story recently refueled by common studies on the similarity of pro-inflammatory and pro-coagulant endotheliopathy in APS and in COVID-19.

Keywords: Animal models; Antiphospholipid syndrome; COVID-19; Endothelium; beta2glycoprotein I.