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

Figure 2

Interaction of monocytes with endothelial cells. Monocyte subpopulations at steady state are involved in maintenance of endothelial integrity by removing MP, AC, and other cellular debris; however, after an inflammatory environment, monocytes may differentially contribute to endothelial damage depending on the subpopulation, kind of stimulus, and endothelium type where immune response is generated. (a) CD14⁺⁺CD16⁻ classical monocytes are preferably adhered to macrovasculature endothelium, patrolling and monitoring large vessels at steady state. Under inflammatory stimuli such as TNF-α, which activates endothelial cells, CD14⁺⁺CD16⁻ monocytes migrate to the inflammation site in response to CCL2 (MCP-1) and amplify the inflammatory reaction. CD14⁺⁺CD16⁺ intermediate monocytes are weakly adhered to both kind of endothelium and are mainly producers of IL-1β and TNF-α after stimulation with TLR4 agonist. (b) CD14⁺CD16⁺⁺ nonclassical monocytes are preferably adhered to microvasculature, patrolling this type of endothelium by interactions with CX3CR1. Depending on the stimulus, for example, in response to bacterial infection or tissue damage, CD14⁺CD16⁺⁺ monocytes can migrate to the inflammation site (by CX3CL1). Please notice that the graph only shows some components of the vascular wall and some membrane proteins that express monocyte subpopulations and endothelial cells.

(a) Macrovasculature.

(b) Microvasculature.