Format

Send to

Choose Destination
Clin Immunol. 2015 Apr;157(2):133-44. doi: 10.1016/j.clim.2015.01.008. Epub 2015 Jan 28.

Accelerated vascular disease in systemic lupus erythematosus: role of macrophage.

Author information

1
Department of Regenerative Medicine and Cell Biology, Medical University of South Carolina, Charleston, SC, USA.
2
Department of Regenerative Medicine and Cell Biology, Medical University of South Carolina, Charleston, SC, USA. Electronic address: hammadsm@musc.edu.

Abstract

Atherosclerosis is a chronic inflammatory condition that is considered a major cause of death worldwide. Striking phenomena of atherosclerosis associated with systemic lupus erythematosus (SLE) is its high incidence in young patients. Macrophages are heterogeneous cells that differentiate from hematopoietic progenitors and reside in different tissues to preserve tissue integrity. Macrophages scavenge modified lipids and play a major role in the development of atherosclerosis. When activated, macrophages secret inflammatory cytokines. This activation triggers apoptosis of cells in the vicinity of macrophages. As such, macrophages play a significant role in tissue remodeling including atherosclerotic plaque formation and rupture. In spite of studies carried on identifying the role of macrophages in atherosclerosis, this role has not been studied thoroughly in SLE-associated atherosclerosis. In this review, we address factors released by macrophages as well as extrinsic factors that may control macrophage behavior and their effect on accelerated development of atherosclerosis in SLE.

KEYWORDS:

Atherosclerosis;; Autoantibodies; Lipoprotein immune complexes;; Lupus;; Macrophage;; Sphingolipids;

PMID:
25638414
PMCID:
PMC4410070
DOI:
10.1016/j.clim.2015.01.008
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Elsevier Science Icon for PubMed Central
Loading ...
Support Center