Abstract
Cardiovascular disease is the leading cause of mortality worldwide, and atherosclerosis the principal factor underlying cardiovascular events. Atherosclerosis is a chronic inflammatory disease characterized by endothelial dysfunction, intimal lipid deposition, smooth muscle cell proliferation, cell apoptosis and necrosis, and local and systemic inflammation, involving key contributions to from innate and adaptive immunity. The balance between proatherogenic inflammatory and atheroprotective anti-inflammatory responses is modulated by a complex network of interactions among vascular components and immune cells, including monocytes, macrophages, dendritic cells, and T, B, and foam cells; these interactions modulate the further progression and stability of the atherosclerotic lesion. In this review, we take a global perspective on existing knowledge about the pathogenesis of immune responses in the atherosclerotic microenvironment and the interplay between the major innate and adaptive immune factors in atherosclerosis. Studies such as this are the basis for the development of new therapies against atherosclerosis.
Highlights
The immune system is divided into two main branches, the innate and adaptive responses Figure 1
Atherosclerotic plaque size is unaffected in LDLR−/− mice, reconstituted with bone marrow depleted of classical DCs (cDCs) by the insertion of diphtheria toxin receptor (DTR) into the cDC-specific Zbtb46 locus [300]
We recently reported that atherosclerosis is increased in ApoE−/− mice upon inhibition of Treg recruitment in early atherosclerotic plaques by the genetic disruption of CCL1, while a similar effect is observed in LDLR−/− mice upon monoclonal antibody blockade of the CCL1-receptor CCR8, suggesting the importance of Treg recruitment in atherosclerosis development [404]
Summary
The immune system is divided into two main branches, the innate and adaptive responses Figure 1. Innate immunity is enacted by cells of the myeloid lineage characterized by their capacity to produce a rapid and nonspecific response as a first line of defense. Innate immune cells mediate host defense responses and inflammation by producing cytokines and chemokines, activating the complement cascade and phagocytosis, or presenting antigens to activate the adaptive immune response. The adaptive response occurs later and depends on the presentation of antigens by antigen presenting cells (APCs) and the cytokine milieu generated by the innate response. Atherosclerosis is a silent disease until increased intimal thickening eventually either diminishes or blocks blood flow, inducing ischemia in downstream tissues, or triggering thrombosis after atherosclerotic plaque rupture [17,18], resulting in myocardial infarction (MI) or stroke [19]
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