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Significance Autoimmunity against phosphatidylethanolamine (PE) was first reported more than three decades ago. Since then, a growing body of literature has documented the prevalence of aPE in a number of clinical conditions including thrombosis and repeated pregnancy loss, but the cellular target of anti-PE antibodies has remained elusive. The study presented here shows that the cellular vulnerability to PE binding is mediated by interactions that occur in the endosomal compartment, which lead to the activation of inflammatory mechanisms. Thus, our results provide knowledge about the pathogenic mechanism of aPE and have important implications for the diagnosis and treatment of this autoimmune condition.

Early endosome as a pathogenic target for antiphosphatidylethanolamine antibodies