Functional profile of activated dendritic cells in unstable atherosclerotic plaque

Erbel, Christian; Sato, Kayoko; Meyer, Frederic B.; Kopecky, Stephen L.; Frye, Robert L.; Goronzy, Jörg J.; Weyand, Cornelia M.

doi:10.1007/s00395-006-0636-x

Cited by 118 publications

(103 citation statements)

References 35 publications

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“…Such mDCs are highly activated and produce the T-cell-attracting chemokines CCL19 and CCL21. 5 Likewise, plasmacytoid DCs (pDCs), a distinct DC subpopulation implicated in regulating antiviral immune responses, populate the inflamed atherosclerotic plaque. 6 Dysfunctional pDCs are now recognized as disease relevant in autoimmune syndromes, such as systemic lupus erythematosus (SLE).…”

Section: Clinical Perspective P 2052mentioning

confidence: 99%

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Synergistic Proinflammatory Effects of the Antiviral Cytokine Interferon-α and Toll-Like Receptor 4 Ligands in the Atherosclerotic Plaque

et al. 2007

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Section: Clinical Perspective P 2052mentioning

confidence: 99%

“…Much less is known about plaque-residing DCs. [3][4][5] When we extrapolate from the prime role DCs play in sensing infections, presenting antigenic peptides to T lymphocytes, and producing chemokines to support lymphoid organogenesis, it is clear that plaqueresiding DCs are versatile and interfere with multiple immunopathways in this specialized tissue niche.…”

mentioning

confidence: 99%

Synergistic Proinflammatory Effects of the Antiviral Cytokine Interferon-α and Toll-Like Receptor 4 Ligands in the Atherosclerotic Plaque

et al. 2007

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“…AS is a commonly recognized inflammatory disease [2][3][4] , although the mechanism of its initiation and progression is not fully understood.…”

Section: Introductionmentioning

confidence: 99%

Angiogenesis Inhibitor, Endostar, Prevents Vasa Vasorum Neovascularization in a Swine Atherosclerosis Model

Xu¹,

Mao²,

Chai

et al. 2015

J Atheroscler Thromb

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Aim:Vasa vasorum neovascularization is a key feature of atherosclerosis (AS) and is strongly associated with inflammatory infiltration, lipid deposition, intraplaque hemorrhage, and hemosiderin deposit. Here we investigate the effects of Endostar, a strong anti-angiogenic drug, on vasa vasorum neovascularization in the experimental porcine model of early AS. Methods: Eighteen adult male Ba-Ma mini pigs were randomized into three groups, with six animals in each group. The pigs in the normal (N) group were fed a normal diet for 18 weeks, without balloon injury surgery. The animals in the atherosclerotic (AS) control and AS Endostar groups were fed a hypercholesterolemic diet for 12 weeks after balloon injury surgery; they received either saline or Endostar for an additional six weeks, while continuing the hypercholesterolemic diet. The atherosclerotic abdominal aorta and levels of serum lipids, TNF-alpha, IL-6, and hs-CRP were analyzed at 18 weeks. Results: The AS group had a significantly higher body weight and serum lipid concentration levels than the N group (p 0.05), confirming the success of the hypercholesterolemic diet. However, no statistical differences were noted between the AS and AS Endostar groups. Histopathology results revealed that vasa vasorum density and intima -media thickness (IMT) had also increased in the AS group compared with those in the N group (p 0.05). The Endostar treatment significantly alleviated AS with decreased vasa vasorum density and IMT (AS vs. AS Endostar, p 0.05). Western blot analysis indicated that the expression of VEGF, -catenin, and TNF-alpha in the atherosclerotic abdominal aorta was considerably reduced by the Endostar treatment. In addition, immunohistochemistry results showed that the angiogenesis markers VEGF and -catenin were predominately localized in endothelial cells of the adventitial vasa vasorum. The levels of the serum inflammatory markers TNF-alpha, hs-CRP, and IL-6 were markedly higher in the AS group than in the N group (p 0.05) but showed no marked difference during the Endostar treatment, suggesting that the local inhibition of angiogenesis was not accompanied by a change in serum inflammatory markers and that the inhibitive effect of Endostar on local TNF-alpha expression could be because of the prevention of vasa vasorum neovascularization. Conclusions: Our results demonstrated that the Endostar treatment inhibited vasa vasorum neovascularization and AS progression in the experimental porcine model of early AS, supporting the role of vasa vasorum neovascularization in the development of AS and the therapeutic potential of antiangiogenesis intervention in AS.

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“…Once the blood cells have attached, chemokines produced in the underlying intima promote the migration into the subendothelial space (5). Plaque-residing APCs such as dendritic cells (DC) 4 then can augment T cell stimulation through the expression of the costimulatory ligands and provide optimal stimulation conditions for T lymphocytes (6).…”

mentioning

confidence: 99%

Inhibition of IL-17A Attenuates Atherosclerotic Lesion Development in ApoE-Deficient Mice

Erbel

Chen²,

Bea³

et al. 2009

The Journal of Immunology

302

243

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Functional profile of activated dendritic cells in unstable atherosclerotic plaque

Cited by 118 publications

References 35 publications

Synergistic Proinflammatory Effects of the Antiviral Cytokine Interferon-α and Toll-Like Receptor 4 Ligands in the Atherosclerotic Plaque

Synergistic Proinflammatory Effects of the Antiviral Cytokine Interferon-α and Toll-Like Receptor 4 Ligands in the Atherosclerotic Plaque

Angiogenesis Inhibitor, Endostar, Prevents Vasa Vasorum Neovascularization in a Swine Atherosclerosis Model

Inhibition of IL-17A Attenuates Atherosclerotic Lesion Development in ApoE-Deficient Mice

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