Perivascular Adipose Tissue Harbors Atheroprotective IgM-Producing B Cells

Srikakulapu, Prasad; Upadhye, Aditi; Rosenfeld, Sam; Marshall, Melissa; McSkimming, Chantel; Hickman, Alexandra; Mauldin, Ileana S.; Ailawadi, Gorav; Lopes, M. Beatriz S.; Taylor, Angela M.; McNamara, Coleen A.

doi:10.3389/fphys.2017.00719

Cited by 49 publications

(72 citation statements)

References 56 publications

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“…B cells contribute to disease pathogenesis in autoimmunity by presenting antigens as well as stimulation via cytokines to T cells [17-21]. B cells also play an immunomodulatory role in regulating the immune response by secreting cytokines that inhibit disease onset and/or progression [10, 22].…”

Section: Discussionmentioning

confidence: 99%

Altered B cells homeostasis in child-onset immunoglobulin A vasculitis

Liu

Jiang

Wang

et al. 2020

Preprint

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46Background: Immunoglobulin A vasculitis (IgAV), also called Henoch-Schönlein purpura, is 47 a systemic small vessels vasculitis with immunoglobulin A1-dominant immune deposits. B-48 cells are a heterogeneous population with unique subsets distinguished by their phenotypes and 49 cytokine production. Here, we explored the status of B cell subsets in patients with IgAV. 50 Methods: Thirty IgAV patients and fifteen age-and sex-matched healthy individuals were 51 enrolled in this study. Fresh blood samples were collected from both healthy and IgAV patients. 52 Upon the distinct expressions of CD3, CD19, CD20, CD38, CD27 and IgD, peripheral blood 53 mononuclear cells (PBMCs) were initially categorized into plasmablasts and memory B cells. 54 Subsequently, using surface markers including CD138 and IgM, and intracellular markers 55 containing IgM and IgG, plasmablasts and memory B cells were further divided into distinct 56 subgroups. A total of eleven populations were detected using multiple flow cytometry. 59 HCs. Only CD3 -CD19 + IgD -CD27 + IgM + B cell counts were reduced in IgAV. The elevated B 60 cell numbers returned to normal after treatment. Plasma and plasmablast B cell numbers 61 correlated with plasma IgA levels. On the contrary, CD3 -CD19 + IgD -CD27 + IgM + B cell 62 numbers were negatively proportional to the plasma IgA levels while naïve B cell numbers 63 correlated with plasma and plasmablast B cell counts.64 Conclusions: We hypothesized that immunoglobulin production was abnormally elevated in 65 IgAV and could be explained by altered B-cell subset homeostasis.66

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Section: Discussionmentioning

confidence: 99%

Altered B cells homeostasis in child-onset immunoglobulin A vasculitis

Liu

Jiang

Wang

et al. 2020

Preprint

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“…While much of the interest in PVAT biology centers on its ability to promote inflammation and atherosclerosis in obesity, interestingly, healthy PVAT may be home to immune cells that attenuate atherosclerosis development. B-1 cell-derived IgM has been shown to attenuate pro-inflammatory cytokine production by M1 macrophages in visceral adipose tissue [29]. Srikakulapu et al [29] demonstrated that in young ApoE-deficient mice, B-1 cells abundantly secreting IgM were present at surprisingly higher numbers in PVAT compared with aorta, and the PVAT B-1/B-2 ratio suggests an anti-inflammatory influence of PVAT.…”

Section: Interplay Between Inflammation and Vascular Function: Potentmentioning

confidence: 99%

“…B-1 cell-derived IgM has been shown to attenuate pro-inflammatory cytokine production by M1 macrophages in visceral adipose tissue [29]. Srikakulapu et al [29] demonstrated that in young ApoE-deficient mice, B-1 cells abundantly secreting IgM were present at surprisingly higher numbers in PVAT compared with aorta, and the PVAT B-1/B-2 ratio suggests an anti-inflammatory influence of PVAT. Furthermore, immunohistochemistry data from human coronary PVAT demonstrated that B cells were found aggregated in close proximity to the coronary artery in fat-associated lymphoid clusters.…”

Section: Interplay Between Inflammation and Vascular Function: Potentmentioning

confidence: 99%

Potential role of perivascular adipose tissue in modulating atherosclerosis

2020

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Perivascular adipose tissue (PVAT) directly juxtaposes the vascular adventitia and contains a distinct mixture of mature adipocytes, preadipocytes, stem cells, and inflammatory cells that communicate via adipocytokines and other signaling mediators with the nearby vessel wall to regulate vascular function. Cross-talk between perivascular adipocytes and the cells in the blood vessel wall is vital for normal vascular function and becomes perturbed in diseases such as atherosclerosis. Perivascular adipocytes surrounding coronary arteries may be primed to promote inflammation and angiogenesis, and PVAT phenotypic changes occurring in the setting of obesity, hyperlipidemia etc., are fundamentally important in determining a pathogenic versus protective role of PVAT in vascular disease. Recent discoveries have advanced our understanding of the role of perivascular adipocytes in modulating vascular function. However, their impact on cardiovascular disease (CVD), particularly in humans, is yet to be fully elucidated. This review will highlight the complex mechanisms whereby PVAT regulates atherosclerosis, with an emphasis on clinical implications of PVAT and emerging strategies for evaluation and treatment of CVD based on PVAT biology.

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“…Antibodies to specific epitopes of oxidized LDL suppress both inflammatory cytokine production and foam cell formation [26,27] .…”

Section: Factors Affecting the Formation Of Foam Cellsmentioning

confidence: 99%

Low density lipoprotein-induced lipid accumulation is a key phenomenon of atherogenesis at the arterial cell level

Orekhov¹,

Myasoedova²

2019

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Lipid accumulation in cells of subendothelial intima and the formation of foam cells is the earliest and the most noticeable manifestation of atherosclerosis at the cellular level. Generally, the foam cell formation is the result of interaction of cell with pro-atherogenic low-density lipoprotein providing cholesterol delivery and anti-atherogenic highdensity lipoprotein providing its efflux. In this review, we discuss possible mechanisms of foam cell formation, the role of intracellular lipid deposition as a trigger of atherosclerotic lesion development, current approaches to diagnostics and strategies for preventing atherosclerosis based on recent knowledge of causes of foam cell formation.

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Perivascular Adipose Tissue Harbors Atheroprotective IgM-Producing B Cells

Cited by 49 publications

References 56 publications

Altered B cells homeostasis in child-onset immunoglobulin A vasculitis

Altered B cells homeostasis in child-onset immunoglobulin A vasculitis

Potential role of perivascular adipose tissue in modulating atherosclerosis

Low density lipoprotein-induced lipid accumulation is a key phenomenon of atherogenesis at the arterial cell level

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