Changes in blood dendritic cell counts in relation to type of coronary artery disease and brachial endothelial cell function

Vré, Emily A. Van; Brussel, Ilse Van; Beeck, Ken Op de; Hoymans, Vicky Y.; Vrints, Christiaan J.; Bult, Hidde; Bosmans, Johan

doi:10.1097/mca.0b013e3283368c0e

Cited by 28 publications

(43 citation statements)

References 26 publications

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“…Some studies reported unchanged counts of pDCs in patients with coronary artery disease (CAD) (Shi et al, 2007) and myocardial infarction (MI) (Wen et al, 2013). Other researchers detected decreased numbers of pDCs in patients with troponin-positive unstable coronary artery syndromes (Van Vré et al, 2006), end-stage heart disease (Athanassopoulos et al, 2004), and advanced CAD (Yilmaz et al, 2009; Van Vré et al, 2010). Furthermore, an inverse correlation between the severity of CAD and pDC numbers was observed (Yilmaz et al, 2009; Van Brussel et al, 2011).…”

Section: Proinflammatory Activities Of Pdcs In Atherosclerosismentioning

confidence: 93%

Plasmacytoid dendritic cells: development, functions, and role in atherosclerotic inflammation

et al. 2014

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Plasmacytoid dendritic cells (pDCs) are a specialized subset of DCs that links innate and adaptive immunity. They sense viral and bacterial pathogens and release high levels of Type I interferons (IFN-I) in response to infection. pDCs were shown to contribute to inflammatory responses in the steady state and in pathology. In atherosclerosis, pDCs are involved in priming vascular inflammation and atherogenesis through production of IFN-I and chemokines that attract inflammatory cells to inflamed sites. pDCs also contribute to the proinflammatory activation of effector T cells, cytotoxic T cells, and conventional DCs. However, tolerogenic populations of pDCs are found that suppress atherosclerosis-associated inflammation through down-regulation of function and proliferation of proinflammatory T cell subsets and induction of regulatory T cells with potent immunomodulatory properties. Notably, atheroprotective tolerogenic DCs could be induced by certain self-antigens or bacterial antigens that suggests for great therapeutic potential of these DCs for development of DC-based anti-atherogenic vaccines.

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Section: Proinflammatory Activities Of Pdcs In Atherosclerosismentioning

confidence: 93%

Plasmacytoid dendritic cells: development, functions, and role in atherosclerotic inflammation

et al. 2014

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“…The amount of circulating precursor DCs is indicative of the immune status of the organism, and decreased blood precursor DC levels have been reported in inflammation-related cardiovascular disorders. Reduced circulating precursor DC numbers in patients with atherosclerosis, myocardial infarction, or stage 3 chronic kidney disease have been associated with enhanced activation and recruitment of mature DCs in vascular lesions, infarcted areas or renal tissue [30,31,32]. Once in the tissue, DCs act as mediators of cardiovascular disease.…”

Section: Novel Immune Cell Subtypes Associated With the Development Omentioning

confidence: 99%

Inflammation and Hypertension: New Understandings and Potential Therapeutic Targets

et al. 2014

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Research studying the role of inflammation in hypertension and cardiovascular disease has flourished in recent years; however, the exact mechanisms by which the activated immune cells lead to the development and maintenance of hypertension remain to be elucidated. The objective of this brief review is to summarize and discuss the most recent findings in the field, with special emphasis on potential therapeutics to treat or prevent hypertension. This review will cover novel immune cell subtypes recently associated to the disease including the novel role of cytokines, toll-like receptors and inflammasomes in hypertension.

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“…42 Several studies furthermore point toward a role of DCs in cholesterol metabolism. In mice overexpressing antiapoptotic Decreased in blood in CAD [24][25][26][27][28] Increased in unstable lesions 20,29 Decreased in blood in CAD [25][26][27][28] Present in atherosclerotic lesions 16,30 Increased in unstable lesions 16,30 Inflammatory amplifiers/ upregulation of TLR4 on cDCs/cytotoxic CD4 + T cells responses 30,31 CAD indicates coronary artery disease; cDC, classical DC; DC, dendritic cell; Flt3, factor fms-like tyrosine kinase 3; MHC, major histocompatibility complex; and pDC, plasmacytoid DC. …”

Section: Dcs Take Up Lipids and Control Cholesterol Homeostasismentioning

confidence: 99%

“…Shi et al 22 MHCII-specific T-cell activation 16,19 Type I interferon production 16 CAD indicates coronary artery disease; cDC, classical DC; CDP, common DC precursor; DC, dendritic cell; Flt3, factor fms-like tyrosine kinase 3; M-CSFR, macrophage colony-stimulating factor receptor; MDP, monocyte-DC precursor; MHC, major histocompatibility complex; pDC, plasmacytoid DC; and ?, under debate. 27 The mechanisms responsible for the decline in blood DCs in atherosclerosis may include an enhanced recruitment to lymphoid organs or sites of inflammation, as suggested by their accumulation in vulnerable lesions, 20 an increased DC turnover, or a decreased production or release from bone marrow. 37 Interestingly, decreased numbers of blood Lin −…”

Section: Circulating Dcs: Biomarkers Of Disease?mentioning

confidence: 99%

Dendritic Cells in Atherosclerosis

Zernecke

2015

ATVB

112

113

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Abstract-Atherosclerotic vascular disease is driven by chronic inflammation involving both innate and adaptive immune responses. Dendritic cells (DCs) are found in healthy arteries and accumulate in atherosclerotic lesions and engage in diverse pathogenic and protective mechanisms during atherogenesis. DCs contribute to early foam cell formation, regulate lipid metabolism, and control pro-and antiatherosclerotic T-cell responses by multifarious mechanisms. We, here, review the roles of DCs and plasmacytoid DCs in experimental models of atherosclerosis and the approaches to target DCs in therapeutic vaccination strategies. We, furthermore, discuss the evidence of the potential function of DCs in human atherosclerosis, and dissect the efforts to harness DC subsets as biomarkers of disease. Finally, we discuss necessary future steps that will help to understand the specific contribution of bona fide DCs in atherosclerosis to move toward novel therapeutic approaches. On the basis of distinct developmental pathways, cDCs are further segregated into cDCs type 1 (cDC1s), encompassing CD8α + DCs in lymphoid and CD103 + DCs in nonlymphoid tissue, and CD11b + cDC2s. Analyses of the entire transcriptome revealed a core cDC gene signature absent from monocytes/macrophages and pDCs that include the genes Zbtb46 and Ccr7.7 CD8α + /CD103 + cDCs were furthermore revealed to express toll like receptor (Tlr) 3 and Xcr1, and to require the transcription factors BATF3, IRF8, Id2 for their development, whereas the differentiation of CD11b + cDCs is controlled by RELB, RBPJ and IRF4. The transcription factor E2-2/Tcf4 is an essential regulator of pDC development. [6][7][8][9][10][11][12] Both cDCs and pDCs depend on the growth factor fms-like tyrosine kinase 3 ligand (Flt3L), and Flt3L-dependence can serve as a surrogate marker for common DC precursor origin. 6,10 In contrast, macrophage colony-stimulating factor 1 receptor + monocytes that circulate in blood and enter tissues under inflammatory conditions, give rise to macrophages and monocyte-derived DCs. It is currently unclear if monocyte-derived DCs and macrophages constitute two distinct lineages, or if they are instead highly plastic cells that acquire different functional modules in response to microenvironmental cues 10 (Table 1). In humans, pDCs and 2 types of cDCs (previously referred to as myeloid DCs), namely CD1c + and CD141 + DCs are discriminated, which are considered homologs of CD11b + and CD8 + /CD103 + DCs in mice, respectively. 8,21 These DC subsets circulate as precursors or in an immature state in blood (Table 2) and originate from hematopoietic stem cells in the bone marrow via either granulocyte macrophage progenitors or multilymphoid progenitors. Human homologs of murine DC precursors remain unidentified. 14 Similar to mice, DCs can be detected in the arterial intima of healthy young individuals, 32 and increased numbers of DCs are found in atherosclerotic lesions 29 using unspecific markers, such as S100, CD1a, or fascin. However, a detailed analysis of the...

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Changes in blood dendritic cell counts in relation to type of coronary artery disease and brachial endothelial cell function

Cited by 28 publications

References 26 publications

Plasmacytoid dendritic cells: development, functions, and role in atherosclerotic inflammation

Plasmacytoid dendritic cells: development, functions, and role in atherosclerotic inflammation

Inflammation and Hypertension: New Understandings and Potential Therapeutic Targets

Dendritic Cells in Atherosclerosis

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