Ana Urzainqui

Our group has described that the leukocyte receptor PSGL-1, the main ligand of P-selectin and responsible for the initial contacts of leukocytes with the endothelium during the extravasation process, is a tolerogenic receptor implicated in maintaining the immune system homeostasis. We reported that PSGL-1 absence promotes the development of an autoimmune syndrome similar to human scleroderma and the absence of P-selectin promotes the development of a lupus-like syndrome. In humans, we found that B cells expressing PSGL-1 belong to the Breg subset; importantly, the expression of PSGL-1 is reduced in B cells of scleroderma patients and thus produce lower level of IL-10. Moreover, lupus patients have reduced expression of P-selectin in the skin vessels. Our current research is now focused in translational studies trying to understand the possible role of PSGL-1 and P-selectin in the pathogenesis of these diseases in humans, searching for alterations in PSGL-1-dependent signaling in monocytes and neutrophils that could be implicated in the pathogenesis of scleroderma, lupus and pulmonary arterial hypertension.