The role of B cells in atherosclerosis

Sage, Andrew P.; Tsiantoulas, Dimitrios; Binder, Christoph J.; Mallat, Ziad

doi:10.1038/s41569-018-0106-9

Cited by 228 publications

(241 citation statements)

References 219 publications

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“…The natural antibody also contains antibodies against blood group antigens (Nydegger et al, 2005). Natural antibodies against oxidized lipids have a protective role in some atherosclerosis models and may be involved in clearance of apoptotic cells (Fereidan-Esfahani et al, 2019;Sage et al, 2019). Neonatal exposure to microbial antigens that stimulate B1 cells leads to life-long changes in the antibody repertoire that may influence the response to future encounters not only with the same microbe but with a range of other microbes and allergens that share glycan determinants (Kearney et al, 2015).…”

Section: Natural Antibody and ''Innate Memory''mentioning

confidence: 99%

B Cell Responses: Cell Interaction Dynamics and Decisions

Cyster

Allen

2019

Cell

674

634

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B cells and the antibodies they produce have a deeply penetrating influence on human physiology. Here, we review current understanding of how B cell responses are initiated; the different paths to generate short-and long-lived plasma cells, germinal center cells, and memory cells; and how each path impacts antibody diversity, selectivity, and affinity. We discuss how basic research is informing efforts to generate vaccines that induce broadly neutralizing antibodies against viral pathogens, revealing the special features associated with allergen-reactive IgE responses and uncovering the antibody-independent mechanisms by which B cells contribute to health and disease.

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Section: Natural Antibody and ''Innate Memory''mentioning

confidence: 99%

B Cell Responses: Cell Interaction Dynamics and Decisions

Cyster

Allen

2019

Cell

674

634

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“…2; Döring et al, 2012), again suggesting a shared pathophysiological continuum between autoimmunity and atherosclerosis. Detailed information on the role of B cells and immunoglobulins in atherogenesis is reviewed elsewhere (Sage et al, 2019;Tsiantoulas et al, 2015).…”

Section: Ecsmentioning

confidence: 99%

Type-I interferons in atherosclerosis

Chen

Tas

Winther

2019

Journal of Experimental Medicine

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The contribution of dyslipidemia and inflammation in atherosclerosis is well established. Along with effective lipid-lowering treatments, the recent success of clinical trials with anti-inflammatory therapies and the accelerated atherosclerosis in many autoimmune diseases suggest that targeting inflammation may open new avenues for the prevention and the treatment for cardiovascular diseases (CVDs). In the past decades, studies have widened the role of type-I interferons (IFNs) in disease, from antivirus defense to autoimmune responses and immuno-metabolic syndromes. While elevated type-I IFN level in serum is associated with CVD incidence in patients with interferonopathies, experimental data have attested that type-I IFNs affect plaque-residing macrophages, potentiate foam cell and extracellular trap formation, induce endothelial dysfunction, alter the phenotypes of dendritic cells and T and B lymphocytes, and lead to exacerbated atherosclerosis outcomes. In this review, we discuss the production and the effects of type-I IFNs in different atherosclerosis-associated cell types from molecular biology studies, animal models, and clinical observations, and the potential of new therapies against type-I IFN signaling for atherosclerosis.

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“…The pathophysiology of atherosclerosis is exceptionally complex and involves inflammation 1 , cellular transdifferentiation 2,3 , and dynamic interactions between a variety of cell types within the vascular wall 4,5 . For example, the phenotypic landscape of VSMCs is increasingly understood to be quite dynamic as these cells often participate in phenotype switching 6 and contribute to the development of extracellular matrix producing cells in atherosclerosis 4 .…”

Section: Introductionmentioning

confidence: 99%

Decoding the transcriptome of atherosclerotic plaque at single-cell resolution

Alsaigh¹,

Evans²,

Frankel

et al. 2020

Preprint

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Atherogenesis involves an interplay of inflammation, tissue remodeling and cellular transdifferentiation (CTD), making it especially difficult to precisely delineate its pathophysiology. Here we examine the single-cell transcriptome of entire atherosclerotic core (AC) plaques and patient-matched proximal adjacent (PA) portions of carotid artery tissue from patients undergoing carotid endarterectomy. We use a novel tissue dissociation strategy, single-cell RNA sequencing, and systems-biology approaches to analyze the transcriptional profiles of six main cell populations and identify key gene drivers of pathogenic biological processes in vascular smooth muscle cells (VSMCs) and endothelial cells (ECs). Our results reveal an anatomic continuum whereby PA cells promote and respond to inflammatory processes and eventually transition through CTD into matrix-secreting cells in the AC. Inflammatory signaling in PA ECs is driven by IL6, while TNFa signaling defines inflammation in both PA ECs and VSMCs. Furthermore, we identify POSTN, SPP1 and IBSP in AC VSMCs, and ITLN1, SCX and S100A4 in AC ECs as key drivers of CTD in the atherosclerotic core. These results establish an anatomic framework for atherogenesis and suggest a site-specific strategy for disruption of disease progression.

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The role of B cells in atherosclerosis

Cited by 228 publications

References 219 publications

B Cell Responses: Cell Interaction Dynamics and Decisions

B Cell Responses: Cell Interaction Dynamics and Decisions

Type-I interferons in atherosclerosis

Decoding the transcriptome of atherosclerotic plaque at single-cell resolution

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