Accelerated exposure of phosphatidylserine on lymphocyte populations from patients with systemic lupus erythematosus or rheumatoid arthritis

To summarise, we have shown that lymphocyte populations from patients with SLE, RA and, to a lesser extent, IBD, exhibit an increased rate of calcium ionophore-stimulated exposure of PS to the cell surface, as evidenced by the increased proportion of responding cells. It is not possible from these experiments, however, to assess whether the rate at which PS is translocated from the inner leaflet on individual cells differs between patients and controls. The cause(s) of the increased rates of PS exposure we have observed remain to be elucidated. Indeed, little is known about the mechanism of PS translocation. Whilst it has been suggested that the protein ABCA1 acts as a PS floppase and rates of PS translocation are reduced in haematopoietic cells from ABCA1-deficient mice (14), as there is no evidence for direct interaction between ABCA1 and PS this protein may act upstream of any translocase. We did not find any significant difference in the level of leukocyte ABCA1 mRNA between patients and controls (not shown). These findings indicate that increased rates of exposure of PS in SLE, RA and IBD may contribute toward the elevated thrombotic risk in each disorder. © 2005 Schattauer GmbH, Stuttgart.