Figure 1 Innate immune responses in atherosclerosis

Slides:

Advertisements

Similar presentations

Statins as Protective Agents for Aortic Endothelial Cells Robert Kreisberg West Liberty State College.

Advertisements

03/06/231 K June /06/232 Atherosclerosis Etiology Classic Risk Factors Dyslipidemia Low HDL Epidemiological Studies (e.g. Framingham) Genetic.

atherosclerosis Jon Yap John A. Burns School of Medicine

Lipoprotein Structure, Function, and Metabolism

Is atherosclerosis a metabolic disease?

Peter Libby, MD The American Journal of Medicine

Figure 3 Neutrophils in liver inflammation

Volume 17, Issue 6, Pages (June 2013)

Figure 3 Altered adaptive immune functions after sepsis

Volume 17, Issue 5, Pages (May 2013)

Figure 2 Main functions of IL-1

Figure 1 Immune mechanisms in liver homeostasis

Nat. Rev. Nephrol. doi: /nrneph

Nat. Rev. Cardiol. doi: /nrcardio

Nat. Rev. Cardiol. doi: /nrcardio

Figure 3 Molecular mechanisms of crystal-induced necroinflammation

Nat. Rev. Cardiol. doi: /nrcardio

Nicholas van Bruggen, Wenjun Ouyang Immunity

Nat. Rev. Nephrol. doi: /nrneph

Nat. Rev. Nephrol. doi: /nrneph

Figure 5 Mechanisms of crystal granuloma formation

Figure 2 Invariant natural killer T (iNKT) cells promote atherogenesis

Figure 2 Mechanism of glycocalyx degradation

Craig H Selzman, MD, Stephanie A Miller, MD, Alden H Harken, MD

Interaction of hypercholesterolemia and inflammation in atherogenesis

Nat. Rev. Cardiol. doi: /nrcardio

Figure 3 Cascade of events leading from AKI to ALI

and obesity-related kidney diseases

Nat. Rev. Nephrol. doi: /nrneph

Nat. Rev. Endocrinol. doi: /nrendo

Nat. Rev. Nephrol. doi: /nrneph

Figure 3 Loss of the glycocalyx leads to podocyte and kidney injury

Figure 3 LDL autoimmunity in atherosclerosis

Arterial wall: structure and function

Figure 4 TNFSF inflammatory activities in tissue cells

Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro

Figure 3 Biologics that attenuate effector responses in the kidney

Figure 1 Heart–brain–kidney interactions control cardiac remodelling

Unraveling the NALP-3/IL-1β Inflammasome

Nat. Rev. Nephrol. doi: /nrneph

Diabetes and atherosclerosis

Inflammatory health effects of indoor and outdoor particulate matter

Nat. Rev. Nephrol. doi: /nrneph

Nat. Rev. Nephrol. doi: /nrneph

Figure 2 Adaptive immunity in atherosclerosis

Lipid core constitution Activated macrophages accumulate lipids

Nat. Rev. Cardiol. doi: /nrcardio

Figure 2 GM-CSF — a key player in inflammation and autoimmunity

Chengcheng Jin, Jorge Henao-Mejia, Richard A. Flavell Cell Metabolism

Figure 3 Regulation of insulin sensitivity by innate immune cells

Figure 1 Sequence of events in the development of autoimmune nephritis

End-stage renal disease, atherosclerosis, and cardiovascular mortality: Is C-reactive protein the missing link? Mustafa Arici, John Walls Kidney International

Volume 5, Issue 3, Pages (December 1998)

Monocyte-Macrophages and T Cells in Atherosclerosis

Nat. Rev. Nephrol. doi: /nrneph

Nat. Rev. Rheumatol. doi: /nrrheum

Figure 3 Underlying mechanisms of TREG cells in atherosclerosis

Figure 2 Protective functions of HDL

Figure 4 Role of chemokines in dendritic cell migration

Atherosclerosis Dr:HAMED ALGHAMDI.

End-stage renal disease, atherosclerosis, and cardiovascular mortality: Is C-reactive protein the missing link? Mustafa Arici, John Walls Kidney International

Figure 1 The role of macrophages in RA

The Biological Role of Inflammation in Atherosclerosis

Macrophages in the Pathogenesis of Atherosclerosis

Do Oxidized Lipoproteins Cause Atherosclerotic Cardiovascular Diseases? Benoit J. Arsenault, PhD, Raphaëlle Bourgeois, MSc, Patrick Mathieu, MD, MSc,

Impaired Lung Function and Risk for Stroke

Damage-associated molecular pattern (DAMP)-induced activation of Toll-like receptors (TLRs). Damage-associated molecular pattern (DAMP)-induced activation.

Atherosclerosis Christopher K. Glass, Joseph L. Witztum Cell

Signal transduction pathways and activation of the innate immune response. Signal transduction pathways and activation of the innate immune response. In.

NF-κB, Inflammation, and Metabolic Disease

Presentation transcript:

Figure 1 Innate immune responses in atherosclerosis Figure 1 | Innate immune responses in atherosclerosis. LDL retention initiates atherosclerosis development. Subendothelial accumulation of lipoproteins leads to upregulation of adhesion molecules on the endothelial surface and recruitment of monocytes to the forming lesion. Monocytes transmigrate into the subendothelial space and differentiate into macrophages in response to macrophage-colony stimulating factor (M-CSF) and granulocyte–macrophage colony stimulating factor (GM-CSF) produced by endothelial cells. Smooth muscle cells can also transdifferentiate into macrophage-like cells. Scavenger-receptor-mediated uptake of lipoproteins by macrophages leads to the formation of foam cells. Cholesterol crystals form in these cells and activate the NACHT, LRR and PYD domains-containing protein 3 inflammasome, resulting in release of IL-1β, which stimulates smooth muscle cells to produce IL-6. Both IL-1β and IL-6 exert proinflammatory effects. In addition, circulating IL-6 might signal to the liver to produce C-reactive protein (CRP). The levels of this biomarker are increased in patients with atherosclerotic cardiovascular disease. Gisterå, A. & Hansson, G. K. (2017) The immunology of atherosclerosis Nat. Rev. Nephrol. doi:10.1038/nrneph.2017.51