Cardiovascular Risk and Psoriasis: Beyond the Traditional Risk Factors Ann G. Coumbe, MD, Marc R. Pritzker, MD, Daniel A. Duprez, MD, PhD  The American Journal of Medicine  Volume 127, Issue 1, Pages 12-18 (January 2014) DOI: 10.1016/j.amjmed.2013.08.013 Copyright © 2014 Elsevier Inc. Terms and Conditions

Figure 1 Mechanisms of accelerated cardiovascular disease trajectory in psoriasis. Antigen presenting cells, such as macrophages and dendritic cells, in the developing plaque or regional lymph node engulf molecules that are then processed and presented on major histone compatibility factor. In the case of atherosclerosis, oxidized low-density lipoprotein not only is processed and presented as antigen but also directly activates the endothelium to express adhesion molecules. Antigen presenting cells also secrete inflammatory cytokines, chemokines, proteases, and radicals that can result in tissue inflammation and tissue damage. T cells of predominant CD4+ subtype are activated if they are able to recognize and bind the presented antigen. If the activated CD4+ cell is a T-helper 1 cell, T-helper 1 cytokines (eg, interferon-γ, tumor necrosis factor-α, and interleukin 2) that propagate the inflammatory state are secreted. If the activated CD4+ cell is a regulatory T cell, anti-inflammatory cytokines (eg, interleukin 10 and transforming growth factor-β) are secreted. LDL = low-density lipoprotein; Th = T-helper; Treg = regulatory T cell. The American Journal of Medicine 2014 127, 12-18DOI: (10.1016/j.amjmed.2013.08.013) Copyright © 2014 Elsevier Inc. Terms and Conditions