Atherosclerosis

2010

DOI: 10.1016/j.atherosclerosis.2010.06.007

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Immunization with a combination of ApoB and HSP60 epitopes significantly reduces early atherosclerotic lesion in Apobtm2SgyLdlrtm1Her/J mice

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Valéria Endrész

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et al.

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Hsp60 and Its Bacterial Counterpart Are Pro-atherogenic Mole1

Discussion1

Hsp60 Tolerization In Atherosclerosis1

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Cited by 41 publications

(40 citation statements)

References 26 publications

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“…Unexpectedly, it was found that several of the generated hybridomas were specific for apo There has also been attempts to further enhance the efficacy of apo B peptide vaccines by including other antigens in the vaccine and Lu et al [37] have reported that immunization with the apo B100 p45 peptide in combination with a peptide derived from HSP60 is more effective than immunization with the apo B100 p45 peptide alone. [39] reported that dendritic cells that have been isolated, pulsed with MDA-LDL in presence of the TLR4 activator LPS and subsequently transferred into apo E -/-mice aggravate atherosclerosis.…”

Section: Targeting Cellular and Humoral Immune Responses Against Apo mentioning

confidence: 99%

Apolipoprotein B100 autoimmunity and atherosclerosis – disease mechanisms and therapeutic potential

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2012

Current Opinion in Lipidology

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Purpose of reviewAdaptive immune responses have been shown to play an important role in the atherosclerotic disease process and both pathogenic and protective immunity has been identified. Apolipoprotein (apo) B100 appears to be a key antigen and novel therapies modulating immune responses against apo B100 have shown promising results in experimental models. This review will discuss recent developments in the mechanistic understanding of apo B100 autoimmunity and approaches taken to use this knowledge for development of novel therapies. Recent findingsIt has recently been shown that not only apo B100 modified by oxidation but also nonmodified apo B100 is targeted by autoimmune responses. This implies that a corresponding set of regulatory T cells with the same antigen specificity must exist and that these cells under normal circumstances are able to prevent autoimmunity against LDL. Recent studies also suggest that the athero-protective effect of apo B100 peptide immunization acts by reenforcing the activity of such cells. SummaryThese novel findings suggest that aggravation of plaque inflammation may occur as result of a local loss of tolerance against LDL in the plaque due to insufficient activity of regulatory T cells. Restoration of lost tolerance represents an interesting novel approach for treatment of cardiovascular disease.

“…Unexpectedly, it was found that several of the generated hybridomas were specific for apo There has also been attempts to further enhance the efficacy of apo B peptide vaccines by including other antigens in the vaccine and Lu et al [37] have reported that immunization with the apo B100 p45 peptide in combination with a peptide derived from HSP60 is more effective than immunization with the apo B100 p45 peptide alone. [39] reported that dendritic cells that have been isolated, pulsed with MDA-LDL in presence of the TLR4 activator LPS and subsequently transferred into apo E -/-mice aggravate atherosclerosis.…”

Section: Targeting Cellular and Humoral Immune Responses Against Apo mentioning

confidence: 99%

Apolipoprotein B100 autoimmunity and atherosclerosis – disease mechanisms and therapeutic potential

¹

,

²

,

³

2012

Current Opinion in Lipidology

View full text Add to dashboard Cite

Purpose of reviewAdaptive immune responses have been shown to play an important role in the atherosclerotic disease process and both pathogenic and protective immunity has been identified. Apolipoprotein (apo) B100 appears to be a key antigen and novel therapies modulating immune responses against apo B100 have shown promising results in experimental models. This review will discuss recent developments in the mechanistic understanding of apo B100 autoimmunity and approaches taken to use this knowledge for development of novel therapies. Recent findingsIt has recently been shown that not only apo B100 modified by oxidation but also nonmodified apo B100 is targeted by autoimmune responses. This implies that a corresponding set of regulatory T cells with the same antigen specificity must exist and that these cells under normal circumstances are able to prevent autoimmunity against LDL. Recent studies also suggest that the athero-protective effect of apo B100 peptide immunization acts by reenforcing the activity of such cells. SummaryThese novel findings suggest that aggravation of plaque inflammation may occur as result of a local loss of tolerance against LDL in the plaque due to insufficient activity of regulatory T cells. Restoration of lost tolerance represents an interesting novel approach for treatment of cardiovascular disease.

“…of atherosclerotic plaque formation and decline of Th1 differentiation [99]. Finally, very recently 2 independent groups showed that immunization with a combination of human HSP60 and apolipoprotein B (apoB) peptides caused a significant reduction of atherosclerotic lesions compared with mice immunized with either human HSP60 or apoB alone [100,101].…”

Section: Hsp60 and Its Bacterial Counterpart Are Pro-atherogenic Molementioning

confidence: 99%

Heat Shock Protein-60 and Risk for Cardiovascular Disease

et al. 2011

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Cardiovascular disease (CVD) is a leading cause of morbidity and mortality worldwide. There is growing evidence that molecular chaperones, many of which are heat shock proteins HSPs, are involved in CVD pathogenesis. In this review we focus on HSP60, the human mitochondrial chaperone that also displays extramitochondrial and extracellular functions. HSP60 is typically cytoprotective but a number of stress conditions determine its conversion to a potentially toxic molecule for cells and tissues. We present illustrative examples of specific subtypes of CVD where HSP60 is implicated in the initiation and/or progression of disease. The data not only indicate a pathogenic role for HSP60 but also its potential as a biomarker with applications for diagnosis, assessing prognosis and response to treatment, as well as for preventing and treating CVD.

“…peptide antigen significantly reduced early atherosclerotic lesions in a mouse model (34). The third, HSP60 was found to regulate some functions of oxidized LDL such as modulation of F-actin capping proteins involved in actin polymerization and macrophage motility (35).…”

Section: Discussionmentioning

confidence: 99%

Nasal or Oral Immunization with GroEL Attenuates Porphyromonas gingivalis-Induced Atherosclerosis

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2013

Int J Oral-Med Sci

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Periodontal disease is one of the most prevalent chronic inflammation of oral cavity, and has been reported to be associated with atherosclerosis. In this study, we assessed the potential of orally or nasally administered recombinant HSP60 from Porphyromonas gingivalis (rGroEL) for prevention of atherosclerosis accelerated by P. gingivalis. Apolipoprotein E deficient spontaneously hyperlipidemic (Apoe shl ) mice were orally or nasally immunized with GroEL and then challenged intravenously with P. gingivalis 381. Atherosclerotic lesions in the proximal aorta of each animal were analyzed histomorphometrically, and the serum concentrations of rGroEL-specific antibodies and cytokines were determined.Although antibody titer sufficient for taking oral or nasal immunity of GroEL under adjuvant-free condition was not obtained, the antibody titers significantly rose by booster effect of P. gingivalis infection. Furthermore, mice given rGroEL orally or nasally followed by P. gingivalis-challenge possessed significant reduction of atherosclerotic plaque accumulation in aortic sinus and lowered the serum MCP-1 and ox-LDL levels compared to nonimmunized, P. gingivalis-challenged mice. These results suggest that oral or nasal immunization with rGroEL could be an effective vaccine for prevention of atherosclerosis accelerated by P. gingivalis.

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