Inflammasome activation of IL-18 results in endothelial progenitor cell dysfunction in systemic lupus erythematosus.

ABSTRACT: Systemic lupus erythematosus (SLE) is an autoimmune disease with heterogeneous manifestations including severe organ damage and vascular dysfunction leading to premature atherosclerosis. IFN-α has been proposed to have an important role in the development of lupus and lupus-related cardiovascular disease, partly by repression of IL-1 pathways leading to impairments in vascular repair induced by endothelial progenitor cells (EPCs) and circulating angiogenic cells (CACs). Counterintuitively, SLE patients also display transcriptional upregulation of the IL-1β/IL-18 processing machinery, the inflammasome. To understand this dichotomy and its impact on SLE-related cardiovascular disease, we examined cultures of human and murine control or lupus EPC/CACs to determine the role of the inflammasome

SUBMITTER: Kahlenberg JM 

PROVIDER: S-EPMC3221936 | biostudies-literature | 2011 Dec

REPOSITORIES: biostudies-literature