Apo material as a trigger for inflammation in systemic lupus erythematosus

Abstract

While several characteristics of systemic lupus erythematosus (SLE) have been investigated, the distinct pathogenetic mechanisms leading to autoimmunity and chronic inflammation are not understood yet. A central role for apo has been implicated in the pathogenesis of SLE and an increased rate of apo or a defective clearance of apo cells have repeatedly been described in SLE patients, which show elevated levels of alpha-interferon (alphaIFN) as well as an enhanced expression of alphaIFN-alpha inducible genes referred to as alphaIFN signature. Recent publications link alphaIFN and apo: apo cell-derived microparticles can directly stimulate plasmacytoid dendritic cells to secret alphaIFN. This review highlights the role of apo material as source for AAg and as a trigger for chronic inflammation in the pathogenesis of SLE.