Deadly tricks to combat atherosclerosis.

Abstract

This editorial refers to ‘Phosphatidylserine liposomesmimic apoptotic cells to attenuate atherosclerosis by expanding polyreactive IgM producing B1a lymphocytes’ by H. Hosseini et al ., pp. 443–452. Cardiovascular disease is still the largest morbidity and mortality issue in Western society. Although current medication has proved effective in reducing cardiovascular disease risk, the need for additional therapeutic options remains. In this issue, Hosseini et al. present an elegant new concept with real bench-to-bedside potential: administration of phosphatidylserine (PS) liposomes to dampen atherosclerosis-related immune responses by mobilizing and expanding atheroprotective B1a cells ( Figure 1 ).1 Figure 1 Apoptotic cells expose phosphatidyl serine (PS) residues on the membrane. Artificial PS-coated liposomes are able to serve as apoptotic-cell-mimics. Administration of apoptotic cells or PS liposomes will promote B1a-cell activity and expansion in the peritoneum, possibly through interaction of PS with TIM-1 receptors. Activated B1a cells will produce increased levels of natural IgM antibodies, which are secreted into the blood where they confer protection against atherosclerotic plaque formation by (i) sequestering oxidized LDL, (ii) inducing elimination of apoptotic cells, and (iii) reducing autoantibody formation, in part by interaction of IgM/OxLDL immune complexes with Fc(micro) receptors on other immune cells. Apoptotic cell and PS liposome dependent B1a cell activation implicates the spleen by a still unknown mechanism; although a role of the recently identified splenic CD138+ B1a cells, representing a major source of IgM, cannot be excluded, it …