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• W2150537701 abstract "HomeArteriosclerosis, Thrombosis, and Vascular BiologyVol. 32, No. 7Refining the Role of B Cells in Atherosclerosis Free AccessEditorialPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessEditorialPDF/EPUBRefining the Role of B Cells in Atherosclerosis Heather M. Perry and Coleen A. McNamara Heather M. PerryHeather M. Perry From the Cardiovascular Division, Department of Medicine and Cardiovascular Research Center, University of Virginia, Charlottesville, VA. Search for more papers by this author and Coleen A. McNamaraColeen A. McNamara From the Cardiovascular Division, Department of Medicine and Cardiovascular Research Center, University of Virginia, Charlottesville, VA. Search for more papers by this author Originally published1 Jul 2012https://doi.org/10.1161/ATVBAHA.112.249235Arteriosclerosis, Thrombosis, and Vascular Biology. 2012;32:1548–1549Lymphocytes and plasma cells have long been detected in the plaque and adventitia of atherosclerotic human arteries,1 yet their role in regulating atherosclerosis has only recently begun to emerge.2–6 Two important studies published in 2002 provide evidence for an atheroprotective role for B cells.3,4 More recently, 2 groups broadened our understanding of B cells and atherosclerosis by providing evidence that B cells can also promote atherosclerosis. Treating atheroscle-rosis-prone mice with an anti-CD20 monoclonal antibody that depleted mature B2, but not B1a cells, attenuated atherosclerosis.5,6 This B2 cell depletion was associated with decreased activated splenic CD4+ T cells, T-cell proliferation, and lesional T cells, suggesting that B2 cells aggravate atherosclerosis through a T-cell–dependent mechanism. Further evidence for an atherogenic role for B2 cells was provided by studies by Kyaw et al6 who found aggravated atherosclerosis in lymphocyte-deficient apolipoprotein E−/−recombinationactivating gene 2−/− common cytokine receptor γ chain-deficient or to B-cell–deficient atherogenic mice after adoptive transfer of 5×106 B2, but not B1, B cells.See accompanying article on page 1573Sage et al7 present another important study on the impact of loss of B2 cells on atherosclerosis by using a genetic strategy of B cell-activating factor receptor (BAFFR) deficiency to deplete B2 cells. BAFFR is a tumor necrosis factor receptor family member that is critical for maintaining mature B2 B cells.8 The authors reconstituted lethally irradiated low-density lipoprotein receptor−/− mice with bone marrow from BAFFR-deficient mice leading to a markedly diminished ability to replenish B2 cells in peripheral lymphoid tissue or blood. This was associated with reduced atherosclerosis, measured by Oil Red O+ staining of the aortic root, after 6 and 8 weeks of high-fat diet. Low-density lipoprotein receptor−/− mice reconstituted with 80% µMT/20% Baffr−/− also had reduced atherosclerosis compared with those reconstituted with control 80% µMT/20% C57BL/6 marrow, providing evidence that it is the loss of BAFFR on B cells mediating this effect. In agreement with their previous findings using anti-CD20 monoclonal antibody depletion of B2 cells,5 they also found that B2 B cell depletion due to BAFFR deficiency reduces the proportion of spleen-derived activated CD4+ T cells and CD4+ T-cell proliferation. Additionally, they found reduced numbers of T cells in aortic roots from Baffr−/− reconstituted mice at 6 (but not 8) weeks of high-fat diet, and at 8 weeks of diet in lesions from µMT/Baffr−/− mice compared with controls, underscoring that in the context of atherosclerosis B2 cells are necessary for activation and proliferation of CD4 T cells. Consistent with the findings of Sage et al,7 Kyaw et al9 also recently published that Baffr−/−apolipoprotein E−/− mice had depletion of mature B2 cells, reduced lesional inflammation, and attenuated atherosclerosis. Taken together, these studies clearly demonstrate that significantly reducing B2 B cell number attenuates atherosclerosis.Yet several important questions about B cell subsets, the context in which they reside and their role in atherosclerosis, remain unanswered. Reduced T-dependent circulating antibodies to modified lipids may be one mechanism of atherosclerosis by which B2 cell depletion attenuated reduced circulating IgG to malondialdehyde-modified low-density lipoprotein was seen with both anti-CD20 monoclonal antibody5,6 and BAFFR deletion7,9 approaches. Recent work provides evidence that splenic B cells from apolipoprotein E−/− mice home to the aorta, and provide atheroprotection.2 Yet, spleen-derived B cells are predominantly B2 cells. Might there be B2 cell–derived atheroprotective B-cell subsets in the spleen that home to the aorta? Indeed, B2 cells can give rise to regulatory B cells that produce the atheroprotective cytokine interleukin-1010 (Figure). Are interleukin-10 producing Bregs atheroprotective? Is it BAFFR-dependent? Or might there be important atheroprotective B1 cells in the spleen that constituitively home to the aorta to promote atheroprotection? Identifying the subsets of B cells in the normal aorta and throughout the progression of disease may provide important clues to the local function of B-cell subsets in regulating atherogenesis. It is also interesting to note that Sage et al7 found a significant reduction in B1b, but not B1a, cell number with BAFFR deficiency. Although the role for B1b cells in atherosclerosis remains elusive, these data suggest that subtypes within the B1 subset may also have unique functions in regulating atherosclerosis (Figure). B1a cells have been reported to be atheroprotective,11 yet recent work describes a new peritoneal B1a-derived B1 cell, innate response activator B cells, that produces the majority of lipopolysaccharide-stimulated granulocyte macrophage-colony stimulating factor in the spleen.12 Granulocyte macrophage-colony stimulating factor stimulates myeloid progenitors in the spleen to differentiate to Ly6Chigh monocytes which traffic to sites of atherosclerosis,13 suggesting that specific contexts can alter B cell subset phenotypes from atheroprotective to atherogenic. Although, whether innate response activator B cells are atherogenic has not been determined.Download figureDownload PowerPointFigure. B-cell subtypes within the B1 and B2 lineages. Conventional B2 B cells promote atherosclerosis. Functions linked to atherogenesis include CD4 T-cell activation and proliferation. The role of Bregs in atherosclerosis is not yet determined. They may attenuate or promote atherosclerosis by secretion of interleukin-10 (IL-10) or IL-12 respectively. Peritoneal B1a cells are atheroprotective. Mechanisms linked to atheroprotection include production of IgM and IL-10. The role of innate response activator B cells (IRA; derived from peritoneal B1a cells) is unknown. Function linked to atherogenesis includes production of granulocyte macrophage-colony stimulating factor (GM-CSF). The role of B1b cells in atherosclerosis is unknown. *Role in atherosclerosis, not yet determined.The study by Sage et al7 adds to the accumulating evidence that depleting B2 cells in mice attenuates atherosclerosis, and supports a role of T cells in this process. The BAFFR could be a target for reducing B2 cells as a strategy to limit atherosclerosis. Yet, a full understanding of the atherogenic and atheroprotective B-cell subsets, the impact of context on their function, and the mechanisms whereby they mediate their effects is needed in order to lead to exciting new strategies whereby immune protection against atherosclerosis could be bolstered without risk of global immune compromise.DisclosuresNone.FootnotesCorrespondence to Coleen A. McNamara, University of Virginia, University of Virginia Health Sciences Center, Box 801394 MR5, Charlottesville, VA 22908. E-mail [email protected]References1. Gerlis LMThe significance of adventitial infiltrations in coronary atherosclerosis.Br Heart J. 1956; 18:166–172.CrossrefMedlineGoogle Scholar2. Doran AC, Lipinski MJ, Oldham SN, Garmey JC, Campbell KA, Skaflen MD, Cutchins A, Lee DJ, Glover DK, Kelly KA, Galkina EV, Ley K, Witztum JL, Tsimikas S, Bender TP, McNamara CAB-cell aortic homing and atheroprotection depend on Id3.Circ Res. 2012; 110:e1–12.LinkGoogle Scholar3. Major AS, Fazio S, Linton MFB-lymphocyte deficiency increases atherosclerosis in LDL receptor-null mice.Arterioscler Thromb Vasc Biol. 2002; 22:1892–1898.LinkGoogle Scholar4. Caligiuri G, Nicoletti A, Poirier B, Hansson GKProtective immunity against atherosclerosis carried by B cells of hypercholesterolemic mice.J Clin Invest. 2002; 109:745–753.CrossrefMedlineGoogle Scholar5. Ait-Oufella H, Herbin O, Bouaziz JD, Binder CJ, Uyttenhove C, Laurans L, Taleb S, Van Vré E, Esposito B, Vilar J, Sirvent J, Van Snick J, Tedgui A, Tedder TF, Mallat ZB cell depletion reduces the development of atherosclerosis in mice.J Exp Med. 2010; 207:1579–1587.CrossrefMedlineGoogle Scholar6. Kyaw T, Tay C, Khan A, Dumouchel V, Cao A, To K, Kehry M, Dunn R, Agrotis A, Tipping P, Bobik A, Toh BHConventional B2 B cell depletion ameliorates whereas its adoptive transfer aggravates atherosclerosis.J Immunol. 2010; 185:4410–4419.CrossrefMedlineGoogle Scholar7. Sage AP, Tsiantoulas D, Baker L, Harrison J, Masters L, Murphy D, Loinard C, Binder CJ, Mallat ZBAFF receptor deficiency reduces the development of atherosclerosis in mice.Arterioscler Thromb Vasc Biol. 2012; 32:1573–1576.LinkGoogle Scholar8. Sasaki Y, Casola S, Kutok JL, Rajewsky K, Schmidt-Supprian MTNF family member B cell-activating factor (BAFF) receptor-dependent and -independent roles for BAFF in B cell physiology.J Immunol. 2004; 173:2245–2252.CrossrefMedlineGoogle Scholar9. Kyaw T, Tay C, Hosseini H, Kanellakis P, Gadowski T, MacKay F, Tipping P, Bobik A, Toh BHDepletion of B2 but not B1a B cells in BAFF receptor-deficient ApoE mice attenuates atherosclerosis by potently ameliorating arterial inflammation.PLoS ONE. 2012; 7:e29371.CrossrefMedlineGoogle Scholar10. Mallat Z, Besnard S, Duriez M, Deleuze V, Emmanuel F, Bureau MF, Soubrier F, Esposito B, Duez H, Fievet C, Staels B, Duverger N, Scherman D, Tedgui AProtective role of interleukin-10 in atherosclerosis.Circ Res. 1999; 85:e17–e24.LinkGoogle Scholar11. Kyaw T, Tay C, Krishnamurthi S, Kanellakis P, Agrotis A, Tipping P, Bobik A, Toh BHB1a B lymphocytes are atheroprotective by secreting natural IgM that increases IgM deposits and reduces necrotic cores in atherosclerotic lesions.Circ Res. 2011; 109:830–840.LinkGoogle Scholar12. Rauch PJ, Chudnovskiy A, Robbins CS, Weber GF, Etzrodt M, Hilgendorf I, Tiglao E, Figueiredo JL, Iwamoto Y, Theurl I, Gorbatov R, Waring MT, Chicoine AT, Mouded M, Pittet MJ, Nahrendorf M, Weissleder R, Swirski FKInnate response activator B cells protect against microbial sepsis.Science. 2012; 335:597–601.CrossrefMedlineGoogle Scholar13. Robbins CS, Chudnovskiy A, Rauch PJ, Figueiredo JL, Iwamoto Y, Gorbatov R, Etzrodt M, Weber GF, Ueno T, van Rooijen N, Mulligan-Kehoe MJ, Libby P, Nahrendorf M, Pittet MJ, Weissleder R, Swirski FKExtramedullary hematopoiesis generates Ly-6C(high) monocytes that infiltrate atherosclerotic lesions.Circulation. 2012; 125:364–374.LinkGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Kyaw T, Peter K, Li Y, Tipping P, Toh B and Bobik A (2017) Cytotoxic lymphocytes and atherosclerosis: significance, mechanisms and therapeutic challenges, British Journal of Pharmacology, 10.1111/bph.13845, 174:22, (3956-3972), Online publication date: 1-Nov-2017. Son Y, Kim H, Yang B, Kim B, Park Y and Kim K (2017) Inhibitory Effects of Methanol Extract from Nardostachys chinensis on 27-hydroxycholesterol-induced Differentiation of Monocytic Cells , Natural Product Sciences, 10.20307/nps.2017.23.4.239, 23:4, (239), . Son Y, Kim B, Park Y and Kim K (2017) Diclofenac Inhibits 27-hydroxycholesterol-induced Differentiation of Monocytic Cells into Mature Dendritic Cells, Immune Network, 10.4110/in.2017.17.3.179, 17:3, (179), . Son Y, Kim B, Eo S, Park Y and Kim K (2016) Dexamethasone Suppresses Oxysterol-Induced Differentiation of Monocytic Cells, Oxidative Medicine and Cellular Longevity, 10.1155/2016/2915382, 2016, (1-8), . Chistiakov D, Orekhov A and Bobryshev Y (2016) ApoA1 and ApoA1-specific self-antibodies in cardiovascular disease, Laboratory Investigation, 10.1038/labinvest.2016.56, 96:7, (708-718), Online publication date: 1-Jul-2016. Huan T, Rong J, Tanriverdi K, Meng Q, Bhattacharya A, McManus D, Joehanes R, Assimes T, McPherson R, Samani N, Erdmann J, Schunkert H, Courchesne P, Munson P, Johnson A, O’Donnell C, Zhang B, Larson M, Freedman J, Levy D and Yang X (2015) Dissecting the Roles of MicroRNAs in Coronary Heart Disease via Integrative Genomic Analyses, Arteriosclerosis, Thrombosis, and Vascular Biology, 35:4, (1011-1021), Online publication date: 1-Apr-2015. Temmerman L and Biessen E (2015) Deadly tricks to combat atherosclerosis, Cardiovascular Research, 10.1093/cvr/cvv133, 106:3, (345-347), Online publication date: 1-Jun-2015. Bene N, Alcaide P, Wortis H and Jaffe I (2014) Mineralocorticoid receptors in immune cells: Emerging role in cardiovascular disease, Steroids, 10.1016/j.steroids.2014.04.005, 91, (38-45), Online publication date: 1-Dec-2014. Huan T, Zhang B, Wang Z, Joehanes R, Zhu J, Johnson A, Ying S, Munson P, Raghavachari N, Wang R, Liu P, Courchesne P, Hwang S, Assimes T, McPherson R, Samani N, Schunkert H, Meng Q, Suver C, O’Donnell C, Derry J, Yang X and Levy D (2013) A Systems Biology Framework Identifies Molecular Underpinnings of Coronary Heart Disease, Arteriosclerosis, Thrombosis, and Vascular Biology, 33:6, (1427-1434), Online publication date: 1-Jun-2013. July 2012Vol 32, Issue 7 Advertisement Article InformationMetrics © 2012 American Heart Association, Inc.https://doi.org/10.1161/ATVBAHA.112.249235PMID: 22699274 Originally publishedJuly 1, 2012 KeywordsB cell-activating factor receptorB cellsatherosclerosisPDF download Advertisement SubjectsPathophysiology" @default.
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