We are analyzing https://link.springer.com/article/10.1007/s00018-013-1289-1.

Title:
Inflammation and immune system interactions in atherosclerosis | Cellular and Molecular Life Sciences
Description:
Cardiovascular disease (CVD) is the leading cause of mortality worldwide, accounting for 16.7 million deaths each year. The underlying cause of the majority of CVD is atherosclerosis. In the past, atherosclerosis was considered to be the result of passive lipid accumulation in the vessel wall. Today’s picture is far more complex. Atherosclerosis is considered a chronic inflammatory disease that results in the formation of plaques in large and mid-sized arteries. Both cells of the innate and the adaptive immune system play a crucial role in its pathogenesis. By transforming immune cells into pro- and anti-inflammatory chemokine- and cytokine-producing units, and by guiding the interactions between the different immune cells, the immune system decisively influences the propensity of a given plaque to rupture and cause clinical symptoms like myocardial infarction and stroke. In this review, we give an overview on the newest insights in the role of different immune cells and subtypes in atherosclerosis.
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Keywords {🔍}

google, scholar, pubmed, cas, atherosclerosis, mice, cells, atherosclerotic, van, thromb, biol, arterioscler, vasc, cell, res, dendritic, circulation, immunol, human, macrophage, lesions, med, clin, role, plaque, invest, apolipoprotein, doicirculationaha, development, hansson, doijci, circ, oxidized, immune, expression, macrophages, exp, lipoprotein, interleukin, inflammation, doi, rev, atherogenesis, immunity, nat, receptor, reduces, witztum, ldl, formation,

Topics {✒️}

il-17a/il-17ra axis plays month download article/chapter oxidized low-density lipoprotein low-grade chronic inflammation tuning t-cell proliferation oxidized low-density lipoproteins antigen-presenting dendritic cells t-cell priming efficacy monoclonal t-cell proliferation mfg-e8-mediated uptake bone marrow-derived cells receptor-mediated lipid uptake partially l-selectin dependent cd4 t-cell-ablated deficient cd40-traf6 signaling macrophage colony-stimulating factor apolipoprotein e-deficient mouse local immune-inflammatory reactions cd8 t-cell migration il-17r signaling disruption apolipoprotein e-deficient mice atp-binding cassette transporters macrophage-mediated proteolytic remodeling immune system deficiency low-density lipoproteins ldl receptor-deficient mice atherosclerotic plaque micro-environment proatherogenic immune responses atherosclerosis review published ifn-gamma potentiates atherosclerosis ldl receptor-null mice apolipoprotein e-knockout mice dendritic cells pulsed cd1d-restricted natural killer th17/treg functional imbalance cd40/cd40l system immune system interactions age-accelerated atherosclerosis correlates monocyte-endothelial cell interactions tgf-beta escape control anti-anti-idiotype antibodies van wanrooij ej modulates plaque composition endoplasmic reticulum stress endoplasmic reticulum stress smooth muscle cells cd1d-dependent activation acute coronary syndrome atherosclerotic lesion formation alternative m2 macrophages

Questions {❓}

Alderman CJ, Bunyard PR, Chain BM, Foreman JC, Leake DS, Katz DR (2002) Effects of oxidised low density lipoprotein on dendritic cells: a possible immunoregulatory component of the atherogenic micro-environment?
Gerdes N, Zirlik A (2011) Co-stimulatory molecules in and beyond co-stimulation—tipping the balance in atherosclerosis?
Harvey EJ, Ramji DP (2005) Interferon-gamma and atherosclerosis: pro- or anti-atherogenic?
Therapeutic strategies targeting inflammation and immunity in atherosclerosis: how to proceed?

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         description:Cardiovascular disease (CVD) is the leading cause of mortality worldwide, accounting for 16.7 million deaths each year. The underlying cause of the majority of CVD is atherosclerosis. In the past, atherosclerosis was considered to be the result of passive lipid accumulation in the vessel wall. Today’s picture is far more complex. Atherosclerosis is considered a chronic inflammatory disease that results in the formation of plaques in large and mid-sized arteries. Both cells of the innate and the adaptive immune system play a crucial role in its pathogenesis. By transforming immune cells into pro- and anti-inflammatory chemokine- and cytokine-producing units, and by guiding the interactions between the different immune cells, the immune system decisively influences the propensity of a given plaque to rupture and cause clinical symptoms like myocardial infarction and stroke. In this review, we give an overview on the newest insights in the role of different immune cells and subtypes in atherosclerosis.
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      headline:Inflammation and immune system interactions in atherosclerosis
      description:Cardiovascular disease (CVD) is the leading cause of mortality worldwide, accounting for 16.7 million deaths each year. The underlying cause of the majority of CVD is atherosclerosis. In the past, atherosclerosis was considered to be the result of passive lipid accumulation in the vessel wall. Today’s picture is far more complex. Atherosclerosis is considered a chronic inflammatory disease that results in the formation of plaques in large and mid-sized arteries. Both cells of the innate and the adaptive immune system play a crucial role in its pathogenesis. By transforming immune cells into pro- and anti-inflammatory chemokine- and cytokine-producing units, and by guiding the interactions between the different immune cells, the immune system decisively influences the propensity of a given plaque to rupture and cause clinical symptoms like myocardial infarction and stroke. In this review, we give an overview on the newest insights in the role of different immune cells and subtypes in atherosclerosis.
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