The role of the vascular dendritic cell network in atherosclerosis

Alberts-Grill, Noah; Denning, Timothy L.; Rezvan, Amir; Jo, Hanjoong

doi:10.1152/ajpcell.00017.2013

Cited by 40 publications

(34 citation statements)

References 253 publications

(445 reference statements)

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“…High levels of cholesterol are associated with obesity, CV diseases and atherosclerosis. Immune response in atherosclerosis is mediated by chemokines which attract monocytes, leading to the innate immune response that characterizes endothelial alterations, from early dysfunction to the stabilization, progression, and rupture of the atherosclerotic plaque [Alberts-Grill et al, 2013]. Cytokines influence tissue and cell physiology, and inflammatory cytokines such as adiponectin, interleukin-6 (IL-6), resistin, and TNF-α are related to metabolic CV risk factors.…”

Section: Discussionmentioning

confidence: 99%

Lipid Profile of Rheumatoid Arthritis Patients Treated with Anti‐Tumor Necrosis Factor‐Alpha Drugs Changes According to Disease Activity and Predicts Clinical Response

Cacciapaglia¹,

Anelli

Rinaldi

et al. 2014

Drug Development Research

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Patients with active rheumatoid arthritis (RA) frequently show an atherogenic lipid profile, which has been linked with the inflammatory reaction. Inflammatory cytokines, and particularly tumor necrosis factor-alpha (TNF-α), are implicated in the pathogenesis of both atherosclerosis and RA, and also involved in the development of the impaired lipid profile detected in active RA. Although anti-TNF-α agents have been proven effective in controlling joint damage and systemic inflammation, controversy remains about the effect of these drugs on the lipid profile; therefore, the aim of our study was to investigate the effect of anti-TNF-α treatment, in combination with disease-modifying anti-rheumatic drugs (DMARDs) and corticosteroid therapy, on the lipid profile of patients with active RA. Our data suggest that the combination anti-TNF-α/DMARDs/steroids do not significantly interfere with the lipid profile of RA patients. However, analysis of clinical response data showed that patients achieving low disease activity or remission seem to have a protective lipid profile, suggesting that better control of inflammation and disease activity can affect lipid metabolism. The available evidence indicates that high inflammation interferes with lipid metabolism, whereas good control of the chronic inflammatory state may positively influence the lipid profile and cardiovascular risk. Low cholesterol levels at baseline could predict a favorable outcome with anti-TNF-α treatment, but these data need to be confirmed by large prospective studies with long-term follow-up.

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Section: Discussionmentioning

confidence: 99%

Lipid Profile of Rheumatoid Arthritis Patients Treated with Anti‐Tumor Necrosis Factor‐Alpha Drugs Changes According to Disease Activity and Predicts Clinical Response

Cacciapaglia¹,

Anelli

Rinaldi

et al. 2014

Drug Development Research

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“…Pro‐inflammatory macrophages are abundant in the plaque lipid and far from anti‐inflammatory macrophages (Chinetti‐Gbaguidi et al, ). Pro‐inflammatory macrophages can enhance the inflammatory activities in the atherosclerotic plagues by the release of IL‐6, IL‐12, and ROS (Adamson & Leitinger, ), while anti‐inflammatory macrophages can inhibit the inflammation in the plaques via efferocytosis (Alberts‐Grill, Denning, Rezvan, & Jo, ). Cholesterol accumulation is accelerated by CCAAT/enhancer‐binding protein delta (CEBPD) only within pro‐inflammatory macrophages of atherosclerotic lesions (Lai et al, ).…”

Section: Inflammation In Icasmentioning

confidence: 99%

Inflammation‐regulatory microRNAs: Valuable targets for intracranial atherosclerosis

Chen

2019

J of Neuroscience Research

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Intracranial atherosclerosis (ICAS) is the most common etiology of ischemic stroke with the highest rate of stroke recurrence. Little is currently known of the association of circulating inflammation-regulatory microRNAs (miRNAs) with ICAS. In this review, we briefly discuss that ICAS is characterized as a dynamic and unstable inflammatory process within intracranial arteries. Then, as a topic of discussion, we mainly concentrate on the following crucial miRNAs (miR-155, miR-27a/b, miR-342-5p, miR-21, miR-124, and miR-223) by virtue of their multiple roles in regulating the progression of atherosclerosis involved with systemic and local inflammatory activities in cerebral arteries. Clinical perspectives of other miRNAs (miR-146a, miR-181b, miR-126, miR-143, and let-7b) in ICAS are also mentioned. In relevance to the inflammatory mechanisms of ICAS, the in-depth knowledge of miRNAs engaged in the progression of intracranial atherosclerotic plaques may provide an approach to a more precise exploration of diagnostic and therapeutic targets for ICAS.

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“…18,19 In kidney biopsies, DC-SIGN + cells stain with other known kidney DC markers (BDCA-1, 8 HLA-DR, 8 CD68, 7,8 and CX3CR1 10 ), show an activated but not fully mature DC phenotype, and are associated with high T cell stimulation capability. 20 Our knowledge of the role of kidney DCs in human allografts is limited to three studies 8,9,21 (Table 1).…”

mentioning

confidence: 99%

Dendritic Cells in Kidney Transplant Biopsy Samples Are Associated with T Cell Infiltration and Poor Allograft Survival

Batal

Serres

Safa

et al. 2015

Journal of the American Society of Nephrology

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Progress in long-term renal allograft survival continues to lag behind the progress in short-term transplant outcomes. Dendritic cells are the most efficient antigen-presenting cells, but surprisingly little attention has been paid to their presence in transplanted kidneys. We used dendritic cell-specific intercellular adhesion molecule-3-grabbing nonintegrin as a marker of dendritic cells in 105 allograft biopsy samples from 105 kidney transplant recipients. High dendritic cell density was associated with poor allograft survival independent of clinical variables. Moreover, high dendritic cell density correlated with greater T cell proliferation and poor outcomes in patients with high total inflammation scores, including inflammation in areas of tubular atrophy. We then explored the association between dendritic cells and histologic variables associated with poor prognosis. Multivariate analysis revealed an independent association between the densities of dendritic cells and T cells. In biopsy samples with high dendritic cell density, electron microscopy showed direct physical contact between infiltrating lymphocytes and cells that have the ultrastructural morphologic characteristics of dendritic cells. The origin of graft dendritic cells was sought in nine sex-mismatched recipients using XY fluorescence in situ hybridization. Whereas donor dendritic cells predominated initially, the majority of dendritic cells in late allograft biopsy samples were of recipient origin. Our data highlight the prognostic value of dendritic cell density in allograft biopsy samples, suggest a new role for these cells in shaping graft inflammation, and provide a rationale for targeting dendritic cell recruitment to promote long-term allograft survival.

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The role of the vascular dendritic cell network in atherosclerosis

Cited by 40 publications

References 253 publications

Lipid Profile of Rheumatoid Arthritis Patients Treated with Anti‐Tumor Necrosis Factor‐Alpha Drugs Changes According to Disease Activity and Predicts Clinical Response

Lipid Profile of Rheumatoid Arthritis Patients Treated with Anti‐Tumor Necrosis Factor‐Alpha Drugs Changes According to Disease Activity and Predicts Clinical Response

Inflammation‐regulatory microRNAs: Valuable targets for intracranial atherosclerosis

Dendritic Cells in Kidney Transplant Biopsy Samples Are Associated with T Cell Infiltration and Poor Allograft Survival

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