Endothelial Alterations in Systemic Lupus Erythematosus and Rheumatoid Arthritis: Potential Effect of Monocyte Interaction

Figure 3

Endothelial alterations in SLE and RA. The binding of autoantibodies to the endothelium and deposition of IC on the microvasculature lead to classical complement and monocyte activation and increased endothelial permeability by alterations of interendothelial junctions. There is also increased cell cytotoxicity by immune cells, which further affects the integrity of the tissue. This endothelial activation and damage produce an acute inflammatory response, which recruit further innate immune cells as neutrophils and other monocytes, induce platelet aggregation with the consequent procoagulant activity and microthrombus formation. These inflammatory events can affect different organs and tissues such as kidney in LES (red) and joint in AR (blue), which contribute to the pathogenesis of these diseases. Finally, the persistence of these inflammatory events could conduce to a macrovascular endothelial alterations and chronic inflammatory process that leads to the development of complications in larger vessels, such as atherosclerosis and cardiovascular disease. Please notice that the graph only shows some components of the vascular wall and some membrane proteins that express monocyte subpopulations and endothelial cells; in addition, it is important to clarify that the graph does not show differences between macro- and microvasculature.