The IMMENSE Study: The Interplay Between iMMune and ENdothelial Cells in Mediating Cardiovascular Risk in Systemic Lupus Erythematosus

Bortoluzzi, Alessandra; Chighizola, Cecilia Beatrice; Fredi, Micaela; Raschi, Elena; Bodio, Caterina; Privitera, Daniela; Gonelli, Arianna; Silvagni, Ettore; Govoni, Marcello; Cavazzana, Ilaria; Airò, Paolo; Meroni, Pier Luigi; Tincani, Anǵela; Franceschini, Franco; Piantoni, Silvia; Casciano, Fabio

doi:10.3389/fimmu.2020.572876

Cited by 14 publications

(17 citation statements)

References 50 publications

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“…Cytokines play a fundamental role in atherosclerosis and associated comorbidities (e.g. psoriasis, SLE, CKD) ( 33 – 37 ). Pro- and anti-atherogenic cytokines have been shown.…”

Section: Pathogenesis Of Atherosclerosismentioning

confidence: 99%

Purinergic Signaling in Controlling Macrophage and T Cell Functions During Atherosclerosis Development

et al. 2021

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Atherosclerosis is a hardening and narrowing of arteries causing a reduction of blood flow. It is a leading cause of death in industrialized countries as it causes heart attacks, strokes, and peripheral vascular disease. Pathogenesis of the atherosclerotic lesion (atheroma) relies on the accumulation of cholesterol-containing low-density lipoproteins (LDL) and on changes of artery endothelium that becomes adhesive for monocytes and lymphocytes. Immunomediated inflammatory response stimulated by lipoprotein oxidation, cytokine secretion and release of pro-inflammatory mediators, worsens the pathological context by amplifying tissue damage to the arterial lining and increasing flow-limiting stenosis. Formation of thrombi upon rupture of the endothelium and the fibrous cup may also occur, triggering thrombosis often threatening the patient’s life. Purinergic signaling, i.e., cell responses induced by stimulation of P2 and P1 membrane receptors for the extracellular nucleotides (ATP, ADP, UTP, and UDP) and nucleosides (adenosine), has been implicated in modulating the immunological response in atherosclerotic cardiovascular disease. In this review we will describe advancements in the understanding of purinergic modulation of the two main immune cells involved in atherogenesis, i.e., monocytes/macrophages and T lymphocytes, highlighting modulation of pro- and anti-atherosclerotic mediated responses of purinergic signaling in these cells and providing new insights to point out their potential clinical significance.

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“…Cytokines play a fundamental role in atherosclerosis and associated comorbidities (e.g. psoriasis, SLE, CKD) ( 33 – 37 ). Pro- and anti-atherogenic cytokines have been shown.…”

Section: Pathogenesis Of Atherosclerosismentioning

confidence: 99%

Purinergic Signaling in Controlling Macrophage and T Cell Functions During Atherosclerosis Development

et al. 2021

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“…Accelerated atherosclerosis is a major cause of morbidity and mortality in SLE patients [ 4 , 5 ]. Risk factors for atherosclerosis in SLE include inflammatory mediators, steroid therapy, and renal injury [ 3 , 6 , 7 ]. There is a need for novel treatment strategies and understanding of mechanisms involved in the pathogenesis of atherosclerosis in SLE.…”

Section: Discussionmentioning

confidence: 99%

“…The atherosclerosis is the main etiology of most cardiovascular diseases [ 6 ]. Cardiovascular diseases due to atherosclerosis is currently regarded as one of the leading causes of death among SLE patients [ 7 ]. The close relationship between SLE and atherosclerosis is well established.…”

Section: Introductionmentioning

confidence: 99%

Mesenchymal stem cell transplantation alleviated atherosclerosis in systemic lupus erythematosus through reducing MDSCs

Yao

et al. 2022

Stem Cell Res Ther

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Objective The mechanism by which mesenchymal stem cell (MSC) transplantation alleviates atherosclerosis in systemic lupus erythematosus (SLE) remains elusive. In this study, we aim to explore the efficacy and mechanism of MSC in ameliorating atherosclerosis in SLE. Methods ApoE−/− and Fas−/− mice on the B6 background were cross-bred to generate SLE mice with atherosclerosis. Myeloid-derived suppressor cells (MDSCs) were sorted and quantified. The apoE−/−Fas−/− mice were either treated with anti-Gr antibody or injected with MDSCs. The lupus-like autoimmunity and atherosclerotic lesions were evaluated. Furthermore, the apoE−/−Fas−/− mice were transplanted with MSCs and lupus-like autoimmunity and atherosclerotic lesions were assessed. Results MDSCs in peripheral blood, spleen, draining lymph nodes increased in apoE−/−Fas−/− mice compared with B6 mice. Moreover, the adoptive transfer of MDSCs aggravated both atherosclerosis and SLE pathologies, whereas depleting MDSCs ameliorated those pathologies in apoE−/−Fas−/− mice. MSC transplantation in apoE−/−Fas−/− mice decreased the percentage of MDSCs, alleviated the typical atherosclerotic lesions, including atherosclerotic lesions in aortae and liver, and reduced serum cholesterol, triglyceride and low-density lipoprotein levels. MSC transplantation also reduced SLE pathologies, including splenomegaly, glomerular lesions, anti-dsDNA antibody in serum, urine protein and serum creatinine. Moreover, MSC transplantation regulated the generation and function of MDSCs through secreting prostaglandin E 2 (PGE2). Conclusion Taken together, these results indicated that the increased MDSCs contributed to atherosclerosis in SLE. MSC transplantation ameliorated the atherosclerosis and SLE through reducing MDSCs by secreting PGE2. Graphical Abstract

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“…• CD4 + CD28 -T cells as markers of immunosenescence, chronic inflammation and endothelial damage (126). Given the pro-inflammatory activity of monocytes and the antiinflammatory effect of HDL, the monocyte/HDL ratio (MHR) has been proposed as a biomarker of systemic inflammation (141) and has been demonstrated to be a prognostic indicator of CV risk in patients with chronic kidney disease (120).…”

Section: Autoantibody Specificitymentioning

confidence: 99%

“…CD4 + CD28 - T cells as markers of immunosenescence, chronic inflammation and endothelial damage ( 126 ).…”

Section: Immune Cellsmentioning

confidence: 99%

Immune mechanisms associated with cardiovascular disease in systemic lupus erythematosus: A path to potential biomarkers

Guzmán‐Martínez

Marañón²

2022

Front. Immunol.

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Systemic lupus erythematosus (SLE) patients display an increased risk of cardiovascular disease (CVD). With the improved clinical management of other classical severe manifestation of the disease, CVD is becoming one of the most relevant complications of SLE, and it is an important factor causing morbidity and mortality. Several immune constituents have been shown to be involved in the pathogenesis of atherosclerosis and endothelial damage in SLE patients, including specific circulating cell populations, autoantibodies, and inflammatory mediators. In this review, we summarize the presentation of CVD in SLE and the role of the autoimmune responses present in SLE patients in the induction of atherogenesis, endothelial impairment and cardiac disease. Additionally, we discuss the utility of these immune mediators as early CVD biomarkers and targets for clinical intervention in SLE patients.

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The IMMENSE Study: The Interplay Between iMMune and ENdothelial Cells in Mediating Cardiovascular Risk in Systemic Lupus Erythematosus

Cited by 14 publications

References 50 publications

Purinergic Signaling in Controlling Macrophage and T Cell Functions During Atherosclerosis Development

Purinergic Signaling in Controlling Macrophage and T Cell Functions During Atherosclerosis Development

Mesenchymal stem cell transplantation alleviated atherosclerosis in systemic lupus erythematosus through reducing MDSCs

Immune mechanisms associated with cardiovascular disease in systemic lupus erythematosus: A path to potential biomarkers

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