title: Inflammatory and immune responses in the arterial media.
abstract: Inflammatory arterial diseases differentially affect the compartments of the vessel wall. The intima and adventitia are commonly involved by the disease process, with luminal and microvascular endothelial cells playing a critical role in the recruitment and activation of leukocytes. In contrast, the avascular media is often spared by immune-mediated disorders. Surprisingly, vascular smooth muscle cells (VSMCs), the predominant and often exclusive cell type of the media, are capable of robust proinflammatory responses to diverse stressors. The multiple cytokines and chemokines produced within the media can profoundly affect macrophage and T cell function, thus amplifying and shaping innate and adaptive immune responses. On the other hand, VSMCs and the extracellular matrix that they produce also display significant anti-inflammatory properties. The balance between the pro- and anti-inflammatory effects of VSMCs and their extracellular matrix versus the strength of the inciting immunologic events determines the pattern of medial pathology. Limitations on the extent of medial infiltration and injury, defined as medial immunoprivilege, are typically seen in arteriosclerotic diseases, such as atherosclerosis and transplant vasculopathy. Conversely, breakdown of medial immunoprivilege that manifests as more intense leukocytic infiltrates, loss of VSMCs, and destruction of the extracellular matrix architecture is a general feature of certain aneurysmal diseases and vasculitides. In this review, we consider the inflammatory and immune functions of VSMCs and how they may lead to medial immunoprivilege or medial inflammation in arterial diseases.
authors.affiliation: From the Departments of Surgery (G.T.) and Immunobiology (J.S.P.), Yale University School of Medicine, New Haven, CT; and Veterans Affairs Connecticut Healthcare System, West Haven, CT (G.T.). george.tellides@yale.edu.
authors.forename: George
authors.initials: G
authors.lastname: Tellides
authors.affiliation: From the Departments of Surgery (G.T.) and Immunobiology (J.S.P.), Yale University School of Medicine, New Haven, CT; and Veterans Affairs Connecticut Healthcare System, West Haven, CT (G.T.).
authors.forename: Jordan S
authors.initials: JS
authors.lastname: Pober
mesh_terms: D000818:Animals; D001158:Arteries / Q000276:immunology* / Q000473:pathology; D004730:Endothelium, Vascular / Q000276:immunology / Q000473:pathology; D006801:Humans; D007111:Immunity, Cellular / Q000276:immunology*; D007249:Inflammation / Q000276:immunology / Q000473:pathology; D009131:Muscle, Smooth, Vascular / Q000276:immunology* / Q000473:pathology; D017540:Tunica Media / Q000276:immunology* / Q000473:pathology
keywords: artery; inflammation; leukocytes; vascular smooth muscle cell