Atherosclerosis

2015

DOI: 10.1016/j.atherosclerosis.2014.12.019

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Disruption of the TSLP-TSLPR-LAP signaling between epithelial and dendritic cells through hyperlipidemia contributes to regulatory T-Cell defects in atherosclerotic mice

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Impact Of Pollutants On Graft Outcome1

Effects Of Cholesterol On Antigen Presenting Cells1

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Cited by 17 publications

(15 citation statements)

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“…Both IL-10 and TGF-β1 have been confirmed to exhibit antiatherogenic properties using different approaches including transfer gene models, knockout models, neutralization, and adenovirus expression vector 2, 3, 9 . In our previous studies, we also found that TGF-β plays a vital role in an oxLDL and thymic stromal lymphopoietin (TSLP) treated atherosclerosis prone model 25, 26, 35 . Because not blocking TGF-β1 signaling but blocking IL-10 signaling significantly abolished the protective effects of IL-37 in a myocardial I/R injury model 12 , and because the ascending range of IL-10 was more significant than TGF-β1 in the present study, the anti-IL-10R mAb was used to clarify whether IL-10 is indispensable for the protective role of IL-37 in atherosclerosis.…”

Section: Discussionmentioning

confidence: 89%

“…The atherosclerotic lesions were quantified in en face preparations of the whole aorta, and the frozen histological sections of the aortic sinus were processed as previously described 25, 26 . After the en face aorta lesion staining, the whole vessel images were captured using a digital camera.…”

Section: Methodsmentioning

confidence: 99%

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Exogenous interleukin 37 ameliorates atherosclerosis via inducing the Treg response in ApoE-deficient mice

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Our previous study indicated that interleukin (IL)-37 is involved in atherosclerosis. In the present study, Anterior tibial arteries were collected from diabetes patients and controls. A histopathological analysis showed that IL-37 was over-expressed in human atherosclerotic plaques. Many types of cells including macrophages, vascular smooth muscle cells (VSMCs), endothelial cells and T lymphocyte expressed IL-37 in human atherosclerotic plaques. ApoE−/− mice were divided into a control group and a recombinant human IL-37-treated group. The IL-37 treatment resulted in a significant decrease in macrophages and CD4+ T lymphocytes and a substantial increase in VSMCs and collagen in atherosclerotic plaques, resulting in a reduction in atherosclerotic plaque size. Furthermore, the IL-37 treatment modulated the CD4+ T lymphocyte activity, including a decrease in T helper cell type 1 (Th1) and Th17 cells and an increase in regulatory T (Treg) cells, and inhibited the maturity of dendritic cells both in vivo and in vitro. In addition, treatment with anti-IL-10 receptor monoclonal antibody abrogated the anti-atherosclerotic effects of IL-37. These data suggest that exogenous IL-37 ameliorates atherosclerosis via inducing the Treg response. IL-37 may be a novel therapeutic to prevent and treat atherosclerotic disease.Atherosclerosis is a chronic inflammatory disease in the arterial wall that is initiated mainly in response to oxidized lipoproteins and controlled by immune system 1-3 . Both innate immunity, which is antigen-and memory-independent, and adaptive immunity, which is antigen-and memory-dependent, are involved in atherosclerosis 2 . The main cell type involved in innate immunity is macrophage. In contrast, T cells and dendritic cells (DCs) are the main cell types in adaptive immunity. Regulating the immune response has been considered as the therapeutic target for the treatment of atherosclerosis 4, 5 .The novel anti-inflammatory cytokine interleukin (IL)-37 is a new member of the IL-1 family, and is only interleukin of this family that is absent in mice 6, 7 . The IL-1 family consists of 11 members, including IL-1α, IL-1β, IL-1Rα, IL-18, IL-33, IL-36Rα, IL-36α, IL-36β, IL-36γ, IL-37 and IL-38 8 . Most of the cytokines of the IL-1 family, such as IL-1 and IL-18, are pro-inflammatory cytokines and significantly promote the development of atherosclerosis 9 . Some, such as IL-1Rα and IL-33, are anti-inflammatory cytokines and efficiently ameliorate atherosclerosis in mice whereas the function of IL-36α remains unclear 9 . Evidence shows that both exogenous

“…Both IL-10 and TGF-β1 have been confirmed to exhibit antiatherogenic properties using different approaches including transfer gene models, knockout models, neutralization, and adenovirus expression vector 2, 3, 9 . In our previous studies, we also found that TGF-β plays a vital role in an oxLDL and thymic stromal lymphopoietin (TSLP) treated atherosclerosis prone model 25, 26, 35 . Because not blocking TGF-β1 signaling but blocking IL-10 signaling significantly abolished the protective effects of IL-37 in a myocardial I/R injury model 12 , and because the ascending range of IL-10 was more significant than TGF-β1 in the present study, the anti-IL-10R mAb was used to clarify whether IL-10 is indispensable for the protective role of IL-37 in atherosclerosis.…”

Section: Discussionmentioning

confidence: 89%

“…The atherosclerotic lesions were quantified in en face preparations of the whole aorta, and the frozen histological sections of the aortic sinus were processed as previously described 25, 26 . After the en face aorta lesion staining, the whole vessel images were captured using a digital camera.…”

Section: Methodsmentioning

confidence: 99%

Exogenous interleukin 37 ameliorates atherosclerosis via inducing the Treg response in ApoE-deficient mice

¹

,

²

,

³

et al. 2017

Self Cite

View full text Add to dashboard Cite

Our previous study indicated that interleukin (IL)-37 is involved in atherosclerosis. In the present study, Anterior tibial arteries were collected from diabetes patients and controls. A histopathological analysis showed that IL-37 was over-expressed in human atherosclerotic plaques. Many types of cells including macrophages, vascular smooth muscle cells (VSMCs), endothelial cells and T lymphocyte expressed IL-37 in human atherosclerotic plaques. ApoE−/− mice were divided into a control group and a recombinant human IL-37-treated group. The IL-37 treatment resulted in a significant decrease in macrophages and CD4+ T lymphocytes and a substantial increase in VSMCs and collagen in atherosclerotic plaques, resulting in a reduction in atherosclerotic plaque size. Furthermore, the IL-37 treatment modulated the CD4+ T lymphocyte activity, including a decrease in T helper cell type 1 (Th1) and Th17 cells and an increase in regulatory T (Treg) cells, and inhibited the maturity of dendritic cells both in vivo and in vitro. In addition, treatment with anti-IL-10 receptor monoclonal antibody abrogated the anti-atherosclerotic effects of IL-37. These data suggest that exogenous IL-37 ameliorates atherosclerosis via inducing the Treg response. IL-37 may be a novel therapeutic to prevent and treat atherosclerotic disease.Atherosclerosis is a chronic inflammatory disease in the arterial wall that is initiated mainly in response to oxidized lipoproteins and controlled by immune system 1-3 . Both innate immunity, which is antigen-and memory-independent, and adaptive immunity, which is antigen-and memory-dependent, are involved in atherosclerosis 2 . The main cell type involved in innate immunity is macrophage. In contrast, T cells and dendritic cells (DCs) are the main cell types in adaptive immunity. Regulating the immune response has been considered as the therapeutic target for the treatment of atherosclerosis 4, 5 .The novel anti-inflammatory cytokine interleukin (IL)-37 is a new member of the IL-1 family, and is only interleukin of this family that is absent in mice 6, 7 . The IL-1 family consists of 11 members, including IL-1α, IL-1β, IL-1Rα, IL-18, IL-33, IL-36Rα, IL-36α, IL-36β, IL-36γ, IL-37 and IL-38 8 . Most of the cytokines of the IL-1 family, such as IL-1 and IL-18, are pro-inflammatory cytokines and significantly promote the development of atherosclerosis 9 . Some, such as IL-1Rα and IL-33, are anti-inflammatory cytokines and efficiently ameliorate atherosclerosis in mice whereas the function of IL-36α remains unclear 9 . Evidence shows that both exogenous

“…Quantitative PCR was performed on ABI PRISM 7900 Sequence Detector system (Applied Biosystems) using SYBR Green I Assay (Takara Biotechnology). Relative gene expression level (the amount of target, normalized to endogenous control gene) was calculated using the comparative Ct method formula 2 −ΔΔCt [ 20 ].…”

Section: Methodsmentioning

confidence: 99%

Elevated Plasma IL‐38 Concentrations in Patients with Acute ST‐Segment Elevation Myocardial Infarction and Their Dynamics after Reperfusion Treatment

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Mediators of Inflammation

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Objective. Recent studies suggest that IL-38 is associated with autoimmune diseases. Furthermore, IL-38 is expressed in human atheromatous plaque. However, the plasma levels of IL-38 in patients with ST-segment elevation myocardial infarction (STEMI) have not yet to be investigated. Methods. On admission, at 24 h, at 48 h, and at 7 days, plasma IL-38, C-reactive protein (CRP), cardiac troponin I (cTNI), and N-terminal of the prohormone brain natriuretic peptide (NT-proBNP) levels were measured and IL-38 gene in peripheral blood mononuclear cells (PBMCs) was detected in STEMI patients. Results. The results showed that plasma IL-38 levels and IL-38 gene expression in PBMCs were significantly increased in STEMI patients compared with control group and were time dependent, peaked at 24 h. In addition, plasma IL-38 levels were dramatically reduced in patients with reperfusion treatment compared with control group. Similar results were also demonstrated with CRP, cTNI, and NT-proBNP levels. Furthermore, IL-38 levels were found to be positively correlated with CRP, cTNI, and NT-proBNP and be weakly negatively correlated with left ventricular ejection fraction (LVEF) in STEMI patients. Conclusions. The results indicate that circulating IL-38 is a potentially novel biomarker for patients with STEMI and IL-38 might be a new target for MI study.

“…Oxidized LDL (ox-LDL) induced autophagosome formation, MHC-II expression, and phosphorylation of SYK in macrophages (70). Oxidized cholesterol promoted the differentiation of monocytic precursors into phenotypically mature dendritic cells (DCs) (71), and treatment of DCs in vitro with ox-LDL was associated with upregulation of the costimulatory molecules CD86 and MHC-II and downregulation of the coinhibitory molecule programmed death ligand-1 (PD-L1) (72). While these data suggest a role for cholesterol in APC function, results have been contradictory for antigen presentation.…”

Section: Impact Of Pollutants On Graft Outcomementioning

confidence: 99%

Impact of environmental factors on alloimmunity and transplant fate

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et al. 2017

Journal of Clinical Investigation

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