Marginal Zone B cells control follicular helper T cell response to high cholesterol diet

Nus, Meritxell; Sage, Andrew S.; Lu, Yuning; Masters, Leanne; Lam, Brian; Newland, Stephen A.; Weller, Sandra; Tsiantoulas, Dimitrios; Raffort, Juliette; Marcus, Damiënne; Finigan, Alison; Kitt, Lauren; Figg, Nichola; Schirmbeck, Reinhold; Kneilling, Manfred; Yeo, Giles S.H.; Binder, Christoph J.; Pompa, José Luis de la; Mallat, Ziad

doi:10.1016/j.atherosclerosis.2017.06.067

Cited by 7 publications

(15 citation statements)

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“…However, with the recognition of novel B-cell subsets, we gained significantly more insight into the actual contribution of B cells to inflammatory disorders. In atherosclerosis, we now know that B1 cells, 19,31 marginal zone B cells, 25 and regulatory B cells 32 can exert protective functions, contrary to follicular B cells that aggravate atherosclerosis. 20,21 Since follicular B cells are in the majority, complete B2 cell depletion has resulted in attenuated atherosclerosis.…”

Section: Discussionmentioning

confidence: 99%

“…Treatment with the BTLA antibody resulted in a B cell pool that is highly enriched in marginal zone B cells and Breg cells, which can both inhibit the CD4 þ T-cell response. 22,25 Hence, we assessed the number of lesional CD4 þ T cells and found a marked reduction in infiltrating CD4 þ T cells in BTLA-treated mice compared with PBS-or isotype-treated mice ( Figure 5A). Corroborating with earlier data, 21 we did not find any relevant numbers of B cells in the lesion at this stage (Supplementary material online, Figure SIX).…”

Section: Activation Of Btla Leads To a Protective T-cell Responsementioning

confidence: 99%

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B- and T-lymphocyte attenuator stimulation protects against atherosclerosis by regulating follicular B cells

Douna

Amersfoort

Schaftenaar

et al. 2019

Cardiovascular Research

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The immune system is strongly involved in atherosclerosis and immune regulation generally leads to attenuated atherosclerosis. Band T-lymphocyte attenuator (BTLA) is a novel co-receptor that negatively regulates the activation of B and T cells; however, there have been no reports of BTLA and its function in atherosclerosis or cardiovascular disease (CVD). We aimed to assess the dominant BTLA expressing leucocyte in CVD patients and to investigate whether BTLA has a functional role in experimental atherosclerosis.

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Section: Discussionmentioning

confidence: 99%

Section: Activation Of Btla Leads To a Protective T-cell Responsementioning

confidence: 99%

B- and T-lymphocyte attenuator stimulation protects against atherosclerosis by regulating follicular B cells

Douna

Amersfoort

Schaftenaar

et al. 2019

Cardiovascular Research

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“…However, removal of spleen depletes not only the B1a population but also the MZ B cells. In a high‐cholesterol environment, it was demonstrated that MZ B cells activated a homoeostatic programme leading to control of inflammatory responses of T follicular helper cells [21]. Furthermore, Grasset et al have highlighted the important role of MZ B cells in protection against atherosclerosis [17].…”

Section: Discussionmentioning

confidence: 99%

“…Also, other groups have studied the impact of splenectomy in atherosclerosis showing that removal of spleen changed the phenotype of the atherosclerotic lesion, with more necrosis and less clearance of apoptotic cells [20]. Recent studies have showed that in hypercholesterolaemic mice, sterile inflammation within the spleen induced protective B‐cell response towards self‐antigens found in oxLDL and apoptotic cells [17] and that high‐cholesterol diet activates an anti‐inflammatory programme specifically in marginal zone (MZ) B cells of the spleen [21].…”

Section: Introductionmentioning

confidence: 99%

Treatment with a Toll‐like Receptor 7 ligand evokes protective immunity against atherosclerosis in hypercholesterolaemic mice

et al. 2020

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Background The interplay between innate and adaptive immunity is central in life‐threatening clinical complications of atherosclerosis such as myocardial infarction and stroke. The specific mechanisms involved and their protective versus detrimental effects in the disease process remain poorly understood. We have previously shown that higher levels of Toll‐like receptor 7 (TLR7) expression in human atherosclerotic lesions are correlated with better patient outcome. Objective In this study, we explored whether TLR7 activation can ameliorate disease in experimental atherosclerosis in mice. Methods Apolipoprotein E deficient mice (Apoe−/−) with established disease were injected for five weeks intraperitoneally with the TLR7 ligand R848. Local effects were evaluated by characterization of the lesion. Systemic effects of the treatment were investigated by immune composition analysis in the spleen and plasma measurements. Results The in vivo treatment arrested lesion progression in the aorta. We also detected expansion of marginal zone B cells and Treg in the spleen together with increased plasma IgM antibodies against oxidized low‐density lipoprotein (oxLDL) and reduced plasma cholesterol levels. These changes were accompanied by increased accumulation of IgM antibodies, decreased necrosis and fewer apoptotic cells in atherosclerotic lesions. Conclusions Our findings show that TLR7 stimulation could ameliorate atherosclerotic lesion burden and reduce plasma cholesterol in Apoe−/− mice. TLR7 stimulation was associated with an atheroprotective B‐cell and Treg response, which may have systemic and local effects within lesions that could prevent arterial lipid accumulation and inflammation.

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“…HCD reduces Tfh cell differentiation and accumulation at the germinal center (GC). This reduction is attributed to the fact that HCD enhances PD-L1-mediated suppression of Tfh cell differentiation and immune response [ 47 ]. Another study did not observe a significant difference in the proportion of Tfh cells between obese and healthy mice, but it showed that obese mice had more IL-17 + Tfh cells and less IFN- γ + Tfh cells [ 48 ].…”

Section: Cholesterol In Cd4 + T Cellsmentioning

confidence: 99%

The Effect of Lipid Metabolism on CD4+ T Cells

Cai

Jin

Chen

2021

Mediators of Inflammation

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CD4+ T cells play a vital role in the adaptive immune system and are involved in the pathogenesis of many diseases, including cancer, autoimmune diseases, and chronic inflammation. As an important mechanism for energy storage, a lot of researches have clarified that metabolism imbalance interacts with immune disorder, and one leads to the other. Lipid metabolism has close relationship with CD4+ T cells. In this review, we discuss fatty acid, cholesterol, prostaglandin, and phospholipid metabolism in CD4+ T cell subsets. Fatty acid β-oxidation (FAO) is activated in Th17 cell to support the proinflammatory function. Cholesterol promotes Th1, Th2, and Treg cell differentiation. In addition to glucose metabolism, lipid metabolism is also very important for immunity. Here, it is highlighted that lipid metabolism regulates CD4+ T cell differentiation and function and is related to diseases.

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Marginal Zone B cells control follicular helper T cell response to high cholesterol diet

Cited by 7 publications

References 0 publications

B- and T-lymphocyte attenuator stimulation protects against atherosclerosis by regulating follicular B cells

B- and T-lymphocyte attenuator stimulation protects against atherosclerosis by regulating follicular B cells

Treatment with a Toll‐like Receptor 7 ligand evokes protective immunity against atherosclerosis in hypercholesterolaemic mice

The Effect of Lipid Metabolism on CD4+ T Cells

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