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Current Vascular Pharmacology

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ISSN (Print): 1570-1611
ISSN (Online): 1875-6212

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Review Article

The Innate Immune System and Cardiovascular Disease in ESKD: Monocytes and Natural Killer Cells

Author(s): Evangelia Dounousi*, Anila Duni, Katerina K. Naka, Georgios Vartholomatos and Carmine Zoccali

Volume 19, Issue 1, 2021

Published on: 27 June, 2020

Page: [63 - 76] Pages: 14

DOI: 10.2174/1570161118666200628024027

Price: $65

Abstract

Adverse innate immune responses have been implicated in several disease processes, including cardiovascular disease (CVD) and chronic kidney disease (CKD). The monocyte subsets natural killer (NK) cells and natural killer T (NKT) cells are involved in innate immunity. Monocytes subsets are key in atherogenesis and the inflammatory cascade occurring in heart failure. Upregulated activity and counts of proinflammatory CD16+ monocyte subsets are associated with clinical indices of atherosclerosis, heart failure syndromes and CKD. Advanced CKD is a complex state of persistent systemic inflammation characterized by elevated expression of proinflammatory and pro-atherogenic CD14++CD16+ monocytes, which are associated with cardiovascular events and death both in the general population and among patients with CKD. Diminished NK cells and NKT cells counts and aberrant activity are observed in both coronary artery disease and end-stage kidney disease. However, evidence of the roles of NK cells and NKT cells in atherogenesis in advanced CKD is circumstantial and remains to be clarified. This review describes the available evidence regarding the roles of specific immune cell subsets in the pathogenesis of CVD in patients with CKD. Future research is expected to further uncover the links between CKD associated innate immune system dysregulation and accelerated CVD and will ideally be translated into therapeutic targets.

Keywords: Proinflammatory monocytes, natural killer cells, natural killer T cells, end-stage kidney disease, atherosclerosis, heart failure.

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[1]
Cooper MD, Herrin BR. How did our complex immune system evolve? Nat Rev Immunol 2010; 10(1): 2-3.
[http://dx.doi.org/10.1038/nri2686] [PMID: 20039476]
[2]
Hato T, Dagher PC. How the innate immune system senses trouble and causes trouble. Clin J Am Soc Nephrol 2015; 10(8): 1459-69.
[http://dx.doi.org/10.2215/CJN.04680514] [PMID: 25414319]
[3]
Okeke EB, Uzonna JE. The pivotal role of regulatory t cells in the regulation of innate immune cells. Front Immunol 2019; 10: 680.
[http://dx.doi.org/10.3389/fimmu.2019.00680] [PMID: 31024539]
[4]
Epelman S, Liu PP, Mann DL. Role of innate and adaptive immune mechanisms in cardiac injury and repair. Nat Rev Immunol 2015; 15(2): 117-29.
[http://dx.doi.org/10.1038/nri3800] [PMID: 25614321]
[5]
de Jager DJ, Grootendorst DC, Jager KJ, et al. Cardiovascular and noncardiovascular mortality among patients starting dialysis. JAMA 2009; 302(16): 1782-9.
[http://dx.doi.org/10.1001/jama.2009.1488] [PMID: 19861670]
[6]
Tripepi G, Mallamaci F, Zoccali C. Inflammation markers, adhesion molecules, and all-cause and cardiovascular mortality in patients with ESRD: searching for the best risk marker by multivariate modeling. J Am Soc Nephrol 2005; 16(Suppl. 1): S83-8.
[http://dx.doi.org/10.1681/ASN.2004110972] [PMID: 15938042]
[7]
Gupta J, Mitra N, Kanetsky PA, et al. Association between albuminuria, kidney function, and inflammatory biomarker profile in CKD in CRIC. Clin J Am Soc Nephrol 2012; 7(12): 1938-46.
[http://dx.doi.org/10.2215/CJN.03500412] [PMID: 23024164]
[8]
Zoccali C. Traditional and emerging cardiovascular and renal risk factors: an epidemiologic perspective. Kidney Int 2006; 70(1): 26-33.
[http://dx.doi.org/10.1038/sj.ki.5000417] [PMID: 16723985]
[9]
Tecklenborg J, Clayton D, Siebert S, Coley SM. The role of the immune system in kidney disease. Clin Exp Immunol 2018; 192(2): 142-50.
[http://dx.doi.org/10.1111/cei.13119] [PMID: 29453850]
[10]
Meier P, Meier R, Blanc E. Influence of CD4+/CD25+ regulatory T cells on atherogenesis in patients with end-stage kidney disease. Expert Rev Cardiovasc Ther 2008; 6(7): 987-97.
[http://dx.doi.org/10.1586/14779072.6.7.987] [PMID: 18666849]
[11]
Hu M, Wang YM, Wang Y, et al. Regulatory T cells in kidney disease and transplantation. Kidney Int 2016; 90(3): 502-14.
[http://dx.doi.org/10.1016/j.kint.2016.03.022] [PMID: 27263492]
[12]
Passlick B, Flieger D, Ziegler-Heitbrock HW. Identification and characterization of a novel monocyte subpopulation in human peripheral blood. Blood 1989; 74(7): 2527-34.
[http://dx.doi.org/10.1182/blood.V74.7.2527.2527] [PMID: 2478233]
[13]
Wright SD, Ramos RA, Tobias PS, Ulevitch RJ, Mathison JC. CD14, a receptor for complexes of lipopolysaccharide (LPS) and LPS binding protein. Science 1990; 249(4975): 1431-3.
[http://dx.doi.org/10.1126/science.1698311] [PMID: 1698311]
[14]
Clarkson SB, Ory PA. CD16. Developmentally regulated IgG Fc receptors on cultured human monocytes. J Exp Med 1988; 167(2): 408-20.
[http://dx.doi.org/10.1084/jem.167.2.408] [PMID: 2964496]
[15]
Zawada AM, Rogacev KS, Rotter B, et al. Super SAGE evidence for CD14++CD16+ monocytes as a third monocyte subset. Blood 2011; 118(12): e50-61.
[http://dx.doi.org/10.1182/blood-2011-01-326827] [PMID: 21803849]
[16]
Ziegler-Heitbrock L, Ancuta P, Crowe S, et al. Nomenclature of monocytes and dendritic cells in blood. Blood 2010; 116(16): e74-80.
[http://dx.doi.org/10.1182/blood-2010-02-258558] [PMID: 20628149]
[17]
Wong KL, Tai JJ, Wong WC, et al. Gene expression profiling reveals the defining features of the classical, intermediate, and nonclassical human monocyte subsets. Blood 2011; 118(5): e16-31.
[http://dx.doi.org/10.1182/blood-2010-12-326355] [PMID: 21653326]
[18]
Boyette LB, Macedo C, Hadi K, et al. Phenotype, function, and differentiation potential of human monocyte subsets. PLoS One 2017; 12(4)e0176460
[http://dx.doi.org/10.1371/journal.pone.0176460] [PMID: 28445506]
[19]
Stansfield BK, Ingram DA. Clinical significance of monocyte heterogeneity. Clin Transl Med 2015; 4: 5.
[http://dx.doi.org/10.1186/s40169-014-0040-3] [PMID: 25852821]
[20]
Belge KU, Dayyani F, Horelt A, et al. The proinflammatory CD14+CD16+DR++ monocytes are a major source of TNF. J Immunol 2002; 168(7): 3536-42.
[http://dx.doi.org/10.4049/jimmunol.168.7.3536] [PMID: 11907116]
[21]
Tacke F, Alvarez D, Kaplan TJ, et al. Monocyte subsets differentially employ CCR2, CCR5, and CX3CR1 to accumulate within atherosclerotic plaques. J Clin Invest 2007; 117(1): 185-94.
[http://dx.doi.org/10.1172/JCI28549] [PMID: 17200718]
[22]
Mosig S, Rennert K, Krause S, et al. Different functions of monocyte subsets in familial hypercholesterolemia: potential function of CD14+ CD16+ monocytes in detoxification of oxidized LDL. FASEB J 2009; 23(3): 866-74.
[http://dx.doi.org/10.1096/fj.08-118240] [PMID: 19001052]
[23]
Schauer D, Starlinger P, Zajc P, et al. Monocytes with angiogenic potential are selectively induced by liver resection and accumulate near the site of liver regeneration. BMC Immunol 2014; 15: 50.
[http://dx.doi.org/10.1186/s12865-014-0050-3] [PMID: 25359527]
[24]
Fujisawa T, Wang K, Niu XL, et al. Angiopoietin-1 promotes atherosclerosis by increasing the proportion of circulating Gr1+ monocytes. Cardiovasc Res 2017; 113(1): 81-9.
[http://dx.doi.org/10.1093/cvr/cvw223] [PMID: 28069704]
[25]
Quintar A, McArdle S, Wolf D, et al. Endothelial protective monocyte patrolling in large arteries intensified by western diet and ather-osclerosis. Circ Res 2017; 120(11): 1789-99.
[http://dx.doi.org/10.1161/CIRCRESAHA.117.310739] [PMID: 28302649]
[26]
Buscher K, Marcovecchio P, Hedrick CC, et al. Patrolling mechanics of nonclassical monocytes in vascular inflammation. Front Cardiovasc Med 2017; 19: 80.
[http://dx.doi.org/10.3389/fcvm.2017.00080]
[27]
Woollard KJ, Geissmann F. Monocytes in atherosclerosis: subsets and functions. Nat Rev Cardiol 2010; 7(2): 77-86.
[http://dx.doi.org/10.1038/nrcardio.2009.228] [PMID: 20065951]
[28]
Mehta NN, Reilly MP. Monocyte mayhem: do subtypes modulate distinct atherosclerosis phenotypes? Circ Cardiovasc Genet 2012; 5(1): 7-9.
[http://dx.doi.org/10.1161/CIRCGENETICS.111.962647] [PMID: 22337925]
[29]
Wheeler JG, Mussolino ME, Gillum RF, Danesh J. Associations between differential leucocyte count and incident coronary heart disease: 1764 incident cases from seven prospective studies of 30,374 individuals. Eur Heart J 2004; 25(15): 1287-92.
[http://dx.doi.org/10.1016/j.ehj.2004.05.002] [PMID: 15288155]
[30]
Rothe G, Gabriel H, Kovacs E, et al. Peripheral blood mononuclear phagocyte subpopulations as cellular markers in hypercholesterolemia. Arterioscler Thromb Vasc Biol 1996; 16(12): 1437-47.
[http://dx.doi.org/10.1161/01.ATV.16.12.1437] [PMID: 8977447]
[31]
Estruch M, Bancells C, Beloki L, Sanchez-Quesada JL, Ordóñez-Llanos J, Benitez S. CD14 and TLR4 mediate cytokine release promoted by electronegative LDL in monocytes. Atherosclerosis 2013; 229(2): 356-62.
[http://dx.doi.org/10.1016/j.atherosclerosis.2013.05.011] [PMID: 23880187]
[32]
Poitou C, Dalmas E, Renovato M, et al. CD14dimCD16+ and CD14+CD16+ monocytes in obesity and during weight loss: relationships with fat mass and subclinical atherosclerosis. Arterioscler Thromb Vasc Biol 2011; 31(10): 2322-30.
[http://dx.doi.org/10.1161/ATVBAHA.111.230979] [PMID: 21799175]
[33]
Rogacev KS, Ulrich C, Blömer L, et al. Monocyte heterogeneity in obesity and subclinical atherosclerosis. Eur Heart J 2010; 31(3): 369-76.
[http://dx.doi.org/10.1093/eurheartj/ehp308] [PMID: 19687164]
[34]
Huang ZS, Chiang BL. Correlation between serum lipid profiles and the ratio and count of the CD16+ monocyte subset in peripheral blood of apparently healthy adults. J Formos Med Assoc 2002; 101(1): 11-7.
[PMID: 11911032]
[35]
Kashiwagi M, Imanishi T, Tsujioka H, et al. Association of monocyte subsets with vulnerability characteristics of coronary plaques as assessed by 64-slice multidetector computed tomography in patients with stable angina pectoris. Atherosclerosis 2010; 212(1): 171-6.
[http://dx.doi.org/10.1016/j.atherosclerosis.2010.05.004] [PMID: 20684824]
[36]
Coen PM, Flynn MG, Markofski MM, Pence BD, Hannemann RE. Adding exercise to rosuvastatin treatment: influence on C-reactive protein, monocyte toll-like receptor 4 expression, and inflammatory monocyte (CD14+CD16+) population. Metabolism 2010; 59(12): 1775-83.
[http://dx.doi.org/10.1016/j.metabol.2010.05.002] [PMID: 20580035]
[37]
Imanishi T, Ikejima H, Tsujioka H, et al. Association of monocyte subset counts with coronary fibrous cap thickness in patients with unstable angina pectoris. Atherosclerosis 2010; 212(2): 628-35.
[http://dx.doi.org/10.1016/j.atherosclerosis.2010.06.025] [PMID: 20615506]
[38]
Nahrendorf M, Swirski FK, Aikawa E, et al. The healing myocardium sequentially mobilizes two monocyte subsets with divergent and complementary functions. J Exp Med 2007; 204(12): 3037-47.
[http://dx.doi.org/10.1084/jem.20070885] [PMID: 18025128]
[39]
Tsujioka H, Imanishi T, Ikejima H, et al. Impact of heterogeneity of human peripheral blood monocyte subsets on myocardial salvage in patients with primary acute myocardial infarction. J Am Coll Cardiol 2009; 54(2): 130-8.
[http://dx.doi.org/10.1016/j.jacc.2009.04.021] [PMID: 19573729]
[40]
Arslan U, Kocaoğlu İ, Falay MY, Balcı M, Duyuler S, Korkmaz A. The association between different monocyte subsets and coronary collateral development. Coron Artery Dis 2012; 23(1): 16-21.
[http://dx.doi.org/10.1097/MCA.0b013e32834df5b3] [PMID: 22045058]
[41]
Tsujioka H, Imanishi T, Ikejima H, et al. Post-reperfusion enhancement of CD14(+)CD16(-) monocytes and microvascular obstruction in ST-segment elevation acute myocardial infarction. Circ J 2010; 74(6): 1175-82.
[http://dx.doi.org/10.1253/circj.CJ-09-1045] [PMID: 20453385]
[42]
van der Laan AM, Hirsch A, Robbers LF, et al. A proinflammatory monocyte response is associated with myocardial injury and impaired functional outcome in patients with ST-segment elevation myocardial infarction: monocytes and myocardial infarction. Am Heart J 2012; 163(1): 57-65.
[http://dx.doi.org/10.1016/j.ahj.2011.09.002] [PMID: 22172437]
[43]
Ozaki Y, Imanishi T, Tanimoto T, et al. Effect of direct renin inhibitor, aliskiren, on peripheral blood monocyte subsets and myocardial salvage in patients with primary acute myocardial infarction. Circ J 2012; 76(6): 1461-8.
[http://dx.doi.org/10.1253/circj.CJ-12-0006] [PMID: 22453004]
[44]
Swirski FK, Nahrendorf M, Etzrodt M, et al. Identification of splenic reservoir monocytes and their deployment to inflammatory sites. Science 2009; 325(5940): 612-6.
[http://dx.doi.org/10.1126/science.1175202] [PMID: 19644120]
[45]
Tapp LD, Shantsila E, Wrigley BJ, Pamukcu B, Lip GY. The CD14++CD16+ monocyte subset and monocyte-platelet interactions in patients with ST-elevation myocardial infarction. J Thromb Haemost 2012; 10(7): 1231-41.
[http://dx.doi.org/10.1111/j.1538-7836.2011.04603.x] [PMID: 22212813]
[46]
Berg KE, Ljungcrantz I, Andersson L, et al. Elevated CD14++CD16- monocytes predict cardiovascular events. Circ Cardiovasc Genet 2012; 5(1): 122-31.
[http://dx.doi.org/10.1161/CIRCGENETICS.111.960385] [PMID: 22238190]
[47]
Rogacev KS, Cremers B, Zawada AM, et al. CD14++CD16+ monocytes independently predict cardiovascular events: a cohort study of 951 patients referred for elective coronary angiography. J Am Coll Cardiol 2012; 60(16): 1512-20.
[http://dx.doi.org/10.1016/j.jacc.2012.07.019] [PMID: 22999728]
[48]
Snaedal S, Heimbürger O, Qureshi AR, et al. Comorbidity and acute clinical events as determinants of C-reactive protein variation in he-modialysis patients: implications for patient survival. Am J Kidney Dis 2009; 53(6): 1024-33.
[http://dx.doi.org/10.1053/j.ajkd.2009.02.008] [PMID: 19394732]
[49]
Panichi V, Rizza GM, Paoletti S, et al. Chronic inflammation and mortality in haemodialysis: effect of different renal replacement therapies. Results from the RISCAVID study. Nephrol Dial Transplant 2008; 23(7): 2337-43.
[http://dx.doi.org/10.1093/ndt/gfm951] [PMID: 18305316]
[50]
Stenvinkel P, Ketteler M, Johnson RJ, et al. IL-10, IL-6, and TNF-alpha: central factors in the altered cytokine network of uremia--the good, the bad, and the ugly. Kidney Int 2005; 67(4): 1216-33.
[http://dx.doi.org/10.1111/j.1523-1755.2005.00200.x] [PMID: 15780075]
[51]
Cohen SD, Phillips TM, Khetpal P, Kimmel PL. Cytokine patterns and survival in haemodialysis patients. Nephrol Dial Transplant 2010; 25(4): 1239-43.
[http://dx.doi.org/10.1093/ndt/gfp625] [PMID: 20007982]
[52]
Satomura A, Endo M, Ohi H, et al. Significant elevations in serum mannose-binding lectin levels in patients with chronic renal failure. Nephron 2002; 92(3): 702-4.
[http://dx.doi.org/10.1159/000064089] [PMID: 12372959]
[53]
Chmielewski M, Bryl E, Marzec L, Aleksandrowicz E, Witkowski JM, Rutkowski B. Expression of scavenger receptor CD36 in chronic renal failure patients. Artif Organs 2005; 29(8): 608-14.
[http://dx.doi.org/10.1111/j.1525-1594.2005.29097.x] [PMID: 16048476]
[54]
Kato S, Chmielewski M, Honda H, et al. Aspects of immune dysfunction in end-stage renal disease. Clin J Am Soc Nephrol 2008; 3(5): 1526-33.
[http://dx.doi.org/10.2215/CJN.00950208] [PMID: 18701615]
[55]
Rogacev KS, Zawada AM, Emrich I, et al. Lower Apo A-I and lower HDL-C levels are associated with higher intermediate CD14++CD16+ monocyte counts that predict cardiovascular events in chronic kidney disease. Arterioscler Thromb Vasc Biol 2014; 34(9): 2120-7.
[http://dx.doi.org/10.1161/ATVBAHA.114.304172] [PMID: 25060791]
[56]
Yoon JW, Pahl MV, Vaziri ND. Spontaneous leukocyte activation and oxygen-free radical generation in end-stage renal disease. Kidney Int 2007; 71(2): 167-72.
[http://dx.doi.org/10.1038/sj.ki.5002019] [PMID: 17136029]
[57]
Liakopoulos V, Jeron A, Shah A, Bruder D, Mertens PR, Gorny X. Hemodialysis-related changes in phenotypical features of monocytes. Sci Rep 2018; 8(1): 13964.
[http://dx.doi.org/10.1038/s41598-018-31889-2] [PMID: 30228352]
[58]
Finney AC, Stokes KY, Pattillo CB, Orr AW. Integrin signaling in atherosclerosis. Cell Mol Life Sci 2017; 74(12): 2263-82.
[http://dx.doi.org/10.1007/s00018-017-2490-4] [PMID: 28246700]
[59]
Moghimpour Bijani F, Vallejo JG, Rezaei N. Toll-like receptor signaling pathways in cardiovascular diseases: challenges and opportunities. Int Rev Immunol 2012; 31(5): 379-95.
[http://dx.doi.org/10.3109/08830185.2012.706761] [PMID: 23083347]
[60]
Kuroki Y, Tsuchida K, Go I, et al. A study of innate immunity in patients with end-stage renal disease: special reference to toll-like receptor-2 and -4 expression in peripheral blood monocytes of hemodialysis patients. Int J Mol Med 2007; 19(5): 783-90.
[http://dx.doi.org/10.3892/ijmm.19.5.783] [PMID: 17390084]
[61]
Koc M, Toprak A, Arikan H, et al. Toll-like receptor expression in monocytes in patients with chronic kidney disease and haemodialysis: relation with inflammation. Nephrol Dial Transplant 2011; 26(3): 955-63.
[http://dx.doi.org/10.1093/ndt/gfq500] [PMID: 20729266]
[62]
Ando M, Shibuya A, Tsuchiya K, Akiba T, Nitta K. Reduced expression of Toll-like receptor 4 contributes to impaired cytokine response of monocytes in uremic patients. Kidney Int 2006; 70(2): 358-62.
[http://dx.doi.org/10.1038/sj.ki.5001548] [PMID: 16738534]
[63]
Gollapudi P, Yoon JW, Gollapudi S, Pahl MV, Vaziri ND. Leukocyte toll-like receptor expression in end-stage kidney disease. Am J Nephrol 2010; 31(3): 247-54.
[http://dx.doi.org/10.1159/000276764] [PMID: 20090311]
[64]
Lorenzen JM, David S, Richter A, et al. TLR-4+ peripheral blood monocytes and cardiovascular events in patients with chronic kidney disease--a prospective follow-up study. Nephrol Dial Transplant 2011; 26(4): 1421-4.
[http://dx.doi.org/10.1093/ndt/gfq758] [PMID: 21239386]
[65]
Combadière C, Potteaux S, Rodero M, et al. Combined inhibition of CCL2, CX3CR1, and CCR5 abrogates Ly6C(hi) and Ly6C(lo) mon-ocytosis and almost abolishes atherosclerosis in hypercholesterolemic mice. Circulation 2008; 117(13): 1649-57.
[http://dx.doi.org/10.1161/CIRCULATIONAHA.107.745091] [PMID: 18347211]
[66]
Muntinghe FL, Verduijn M, Zuurman MW, et al. CCR5 deletion protects against inflammation-associated mortality in dialysis patients. J Am Soc Nephrol 2009; 20(7): 1641-9.
[http://dx.doi.org/10.1681/ASN.2008040432] [PMID: 19389855]
[67]
Okumoto S, Taniguchi Y, Nakashima A, et al. C-C chemokine receptor 2 expression by circulating monocytes influences atherosclerosis in patients on chronic hemodialysis. Ther Apher Dial 2009; 13(3): 205-12.
[http://dx.doi.org/10.1111/j.1744-9987.2009.00658.x] [PMID: 19527467]
[68]
Schepers E, Houthuys E, Dhondt A, et al. Transcriptome analysis in patients with chronic kidney disease on hemodialysis disclosing a key role for CD16+CX3CR1+ monocytes. PLoS One 2015; 10(4)e0121750
[http://dx.doi.org/10.1371/journal.pone.0121750] [PMID: 25830914]
[69]
Metzger R, Bohle RM, Chumachenko P, Danilov SM, Franke FE. CD143 in the development of atherosclerosis. Atherosclerosis 2000; 150(1): 21-31.
[http://dx.doi.org/10.1016/S0021-9150(99)00354-8] [PMID: 10781632]
[70]
Trojanowicz B, Ulrich C, Kohler F, et al. Monocytic angiotensin-converting enzyme 2 relates to atherosclerosis in patients with chronic kidney disease. Nephrol Dial Transplant 2017; 32(2): 287-98.
[PMID: 28186543]
[71]
Ulrich C, Heine GH, Garcia P, et al. Increased expression of monocytic angiotensin-converting enzyme in dialysis patients with cardi-ovascular disease. Nephrol Dial Transplant 2006; 21(6): 1596-602.
[http://dx.doi.org/10.1093/ndt/gfl008] [PMID: 16476718]
[72]
Ulrich C, Seibert E, Heine GH, Fliser D, Girndt M. Monocyte angiotensin converting enzyme expression may be associated with athero-sclerosis rather than arteriosclerosis in hemodialysis patients. Clin J Am Soc Nephrol 2011; 6(3): 505-11.
[http://dx.doi.org/10.2215/CJN.06870810] [PMID: 21127137]
[73]
Ulrich C, Heine GH, Seibert E, Fliser D, Girndt M. Circulating monocyte subpopulations with high expression of angiotensin-converting enzyme predict mortality in patients with end-stage renal disease. Nephrol Dial Transplant 2010; 25(7): 2265-72.
[http://dx.doi.org/10.1093/ndt/gfq012] [PMID: 20150168]
[74]
Heine GH, Ortiz A, Massy ZA, et al. European renal and cardiovascular medicine (EURECA m) working group of the European renal association-European dialysis and transplant association (ERA-EDTA). Monocyte subpopulations and cardiovascular risk in chronic kidney disease. Nat Rev Nephrol 2012; 8(6): 362-9.
[http://dx.doi.org/10.1038/nrneph.2012.41] [PMID: 22410492]
[75]
Heine GH, Ulrich C, Seibert E, et al. CD14(++)CD16+ monocytes but not total monocyte numbers predict cardiovascular events in dialysis patients. Kidney Int 2008; 73(5): 622-9.
[http://dx.doi.org/10.1038/sj.ki.5002744] [PMID: 18160960]
[76]
Rogacev KS, Seiler S, Zawada AM, et al. CD14++CD16+ monocytes and cardiovascular outcome in patients with chronic kidney disease. Eur Heart J 2011; 32(1): 84-92.
[http://dx.doi.org/10.1093/eurheartj/ehq371] [PMID: 20943670]
[77]
Jeng Y, Lim PS, Wu MY, et al. Proportions of proinflammatory monocytes are important predictors of mortality risk in hemodialysis patients. Mediators Inflamm 2017; 20171070959
[http://dx.doi.org/10.1155/2017/1070959] [PMID: 29200664]
[78]
de Sequera P, Corchete E, Bohorquez L, et al. Residual Renal Function in Hemodialysis and Inflammation. Ther Apher Dial 2017; 21(6): 592-8.
[http://dx.doi.org/10.1111/1744-9987.12576] [PMID: 28971592]
[79]
Chiu YL, Shu KH, Yang FJ, et al. A comprehensive characterization of aggravated aging-related changes in T lymphocytes and monocytes in end-stage renal disease: the iESRD study. Immun Ageing 2018; 15: 27.
[http://dx.doi.org/10.1186/s12979-018-0131-x] [PMID: 30455721]
[80]
Sester U, Sester M, Heine G, Kaul H, Girndt M, Köhler H. Strong depletion of CD14(+)CD16(+) monocytes during haemodialysis treatment. Nephrol Dial Transplant 2001; 16(7): 1402-8.
[http://dx.doi.org/10.1093/ndt/16.7.1402] [PMID: 11427632]
[81]
Nockher WA, Wiemer J, Scherberich JE. Haemodialysis monocytopenia: differential sequestration kinetics of CD14+CD16+ and CD14++ blood monocyte subsets. Clin Exp Immunol 2001; 123(1): 49-55.
[http://dx.doi.org/10.1046/j.1365-2249.2001.01436.x] [PMID: 11167997]
[82]
Kawanaka N, Nagake Y, Yamamura M, Makino H. Expression of Fc gamma receptor III (CD16) on monocytes during hemodialysis in patients with chronic renal failure. Nephron 2002; 90(1): 64-71.
[http://dx.doi.org/10.1159/000046316] [PMID: 11744807]
[83]
Rogacev KS, Ziegelin M, Ulrich C, et al. Haemodialysis-induced transient CD16+ monocytopenia and cardiovascular outcome. Nephrol Dial Transplant 2009; 24(11): 3480-6.
[http://dx.doi.org/10.1093/ndt/gfp287] [PMID: 19586969]
[84]
den Hoedt CH, Bots ML, Grooteman MPC, et al. Online hemodiafiltration reduces systemic inflammation compared to low-flux hemo-dialysis. Kidney Int 2014; 86(2): 423-32.
[http://dx.doi.org/10.1038/ki.2014.9] [PMID: 24552852]
[85]
Carracedo J, Merino A, Nogueras S, et al. On-line hemodiafiltration reduces the proinflammatory CD14+CD16+ monocyte-derived den-dritic cells: A prospective, crossover study. J Am Soc Nephrol 2006; 17(8): 2315-21.
[http://dx.doi.org/10.1681/ASN.2006020105] [PMID: 16825330]
[86]
Kim HW, Yang HN, Kim MG, et al. Microinflammation in hemodialysis patients is associated with increased CD14 CD16(+) proinflammatory monocytes: possible modification by on-line hemodiafiltration. Blood Purif 2011; 31(4): 281-8.
[http://dx.doi.org/10.1159/000321889] [PMID: 21242682]
[87]
Ariza F, Merino A, Carracedo J, et al. Post-dilution high convective transport improves microinflammation and endothelial dysfunction independently of the technique. Blood Purif 2013; 35(4): 270-8.
[http://dx.doi.org/10.1159/000350611] [PMID: 23689471]
[88]
Bolasco P, Spiga P, Arras M, Murtas S, La Nasa G. Could there be haemodynamic stress effects on pro-inflammatory CD14+ CD16+ monocytes during convective-diffusive treatments? A prospective randomized controlled trial. Blood Purif 2019; 47(4): 385-94.
[http://dx.doi.org/10.1159/000494711] [PMID: 30602156]
[89]
Merino A, Portolés J, Selgas R, et al. Effect of different dialysis modalities on microinflammatory status and endothelial damage. Clin J Am Soc Nephrol 2010; 5(2): 227-34.
[http://dx.doi.org/10.2215/CJN.03260509] [PMID: 20056757]
[90]
Ulrich C, Heine GH, Gerhart MK, Köhler H, Girndt M. Proinflammatory CD14+CD16+ monocytes are associated with subclinical ath-erosclerosis in renal transplant patients. Am J Transplant 2008; 8(1): 103-10.
[PMID: 18021284]
[91]
Sekerkova A, Krepsova E, Brabcova E, et al. CD14+CD16+ and CD14+CD163+ monocyte subpopulations in kidney allograft trans-plantation. BMC Immunol 2014; 15: 4.
[http://dx.doi.org/10.1186/1471-2172-15-4] [PMID: 24499053]
[92]
Rogacev KS, Zawada AM, Hundsdorfer J, et al. Immunosuppression and monocyte subsets. Nephrol Dial Transplant 2015; 30(1): 143-53.
[http://dx.doi.org/10.1093/ndt/gfu315] [PMID: 25313167]
[93]
Wrigley BJ, Lip GY, Shantsila E. The role of monocytes and inflammation in the pathophysiology of heart failure. Eur J Heart Fail 2011; 13(11): 1161-71.
[http://dx.doi.org/10.1093/eurjhf/hfr122] [PMID: 21952932]
[94]
Vaduganathan M, Greene SJ, Butler J, et al. The immunological axis in heart failure: importance of the leukocyte differential. Heart Fail Rev 2013; 18(6): 835-45.
[http://dx.doi.org/10.1007/s10741-012-9352-9] [PMID: 23054221]
[95]
Frantz S, Falcao-Pires I, Balligand JL, et al. The innate immune system in chronic cardiomyopathy: a European society of cardiology (ESC) scientific statement from the working group on myocardial function of the ESC. Eur J Heart Fail 2018; 20(3): 445-59.
[http://dx.doi.org/10.1002/ejhf.1138] [PMID: 29333691]
[96]
Hamid T, Gu Y, Ortines RV, et al. Divergent tumor necrosis factor receptor-related remodeling responses in heart failure: role of nuclear factor-kappaB and inflammatory activation. Circulation 2009; 119(10): 1386-97.
[http://dx.doi.org/10.1161/CIRCULATIONAHA.108.802918] [PMID: 19255345]
[97]
Putko BN, Wang Z, Lo J, et al. Alberta HEART Investigators. Circulating levels of tumor necrosis factor-alpha receptor 2 are increased in heart failure with preserved ejection fraction relative to heart failure with reduced ejection fraction: evidence for a divergence in pathophysiology. PLoS One 2014; 9(6)e99495
[http://dx.doi.org/10.1371/journal.pone.0099495] [PMID: 24923671]
[98]
Tsutamoto T, Hisanaga T, Wada A, et al. Interleukin-6 spillover in the peripheral circulation increases with the severity of heart failure, and the high plasma level of interleukin-6 is an important prognostic predictor in patients with congestive heart failure. J Am Coll Cardiol 1998; 31(2): 391-8.
[http://dx.doi.org/10.1016/S0735-1097(97)00494-4] [PMID: 9462584]
[99]
Sager HB, Hulsmans M, Lavine KJ, et al. Proliferation and recruitment contribute to myocardial macrophage expansion in chronic heart failure. Circ Res 2016; 119(7): 853-64.
[http://dx.doi.org/10.1161/CIRCRESAHA.116.309001] [PMID: 27444755]
[100]
Bajpai G, Schneider C, Wong N, et al. The human heart contains distinct macrophage subsets with divergent origins and functions. Nat Med 2018; 24(8): 1234-45.
[http://dx.doi.org/10.1038/s41591-018-0059-x] [PMID: 29892064]
[101]
Ma Y, Zhang X, Bao H, et al. Toll-like receptor (TLR) 2 and TLR4 differentially regulate doxorubicin induced cardiomyopathy in mice. PLoS One 2012; 7(7)e40763
[http://dx.doi.org/10.1371/journal.pone.0040763] [PMID: 22808256]
[102]
Satoh M, Shimoda Y, Maesawa C, et al. Activated toll-like receptor 4 in monocytes is associated with heart failure after acute myocardial infarction. Int J Cardiol 2006; 109(2): 226-34.
[http://dx.doi.org/10.1016/j.ijcard.2005.06.023] [PMID: 16051384]
[103]
Unger ED, Dubin RF, Deo R, et al. Association of chronic kidney disease with abnormal cardiac mechanics and adverse outcomes in patients with heart failure and preserved ejection fraction. Eur J Heart Fail 2016; 18(1): 103-12.
[http://dx.doi.org/10.1002/ejhf.445] [PMID: 26635076]
[104]
Lindman BR, Dávila-Román VG, Mann DL, et al. Cardiovascular phenotype in HFpEF patients with or without diabetes: a RELAX trial ancillary study. J Am Coll Cardiol 2014; 64(6): 541-9.
[http://dx.doi.org/10.1016/j.jacc.2014.05.030] [PMID: 25104521]
[105]
Franssen C, Chen S, Unger A, et al. Myocardial microvascular inflammatory endothelial activation in heart failure with preserved ejection fraction. JACC Heart Fail 2016; 4(4): 312-24.
[http://dx.doi.org/10.1016/j.jchf.2015.10.007] [PMID: 26682792]
[106]
Glezeva N, Voon V, Watson C, et al. Exaggerated inflammation and monocytosis associate with diastolic dysfunction in heart failure with preserved ejection fraction: evidence of M2 macrophage activation in disease pathogenesis. J Card Fail 2015; 21(2): 167-77.
[http://dx.doi.org/10.1016/j.cardfail.2014.11.004] [PMID: 25459685]
[107]
Gutiérrez OM, Januzzi JL, Isakova T, et al. Fibroblast growth factor 23 and left ventricular hypertrophy in chronic kidney disease. Circulation 2009; 119(19): 2545-52.
[http://dx.doi.org/10.1161/CIRCULATIONAHA.108.844506] [PMID: 19414634]
[108]
Richter M, Lautze HJ, Walther T, Braun T, Kostin S, Kubin T. The failing heart is a major source of circulating FGF23 via oncostatin M receptor activation. J Heart Lung Transplant 2015; 34(9): 1211-4.
[http://dx.doi.org/10.1016/j.healun.2015.06.007] [PMID: 26267742]
[109]
Wang L, Zhang YL, Lin QY, et al. CXCL1-CXCR2 axis mediates angiotensin II-induced cardiac hypertrophy and remodelling through regulation of monocyte infiltration. Eur Heart J 2018; 39(20): 1818-31.
[http://dx.doi.org/10.1093/eurheartj/ehy085] [PMID: 29514257]
[110]
Han YL, Li YL, Jia LX, et al. Reciprocal interaction between macrophages and T cells stimulates IFN-γ and MCP-1 production in Ang II-induced cardiac inflammation and fibrosis. PLoS One 2012; 7(5)e35506
[http://dx.doi.org/10.1371/journal.pone.0035506] [PMID: 22567105]
[111]
Wang L, Li YL, Zhang CC, et al. Inhibition of Toll-like receptor 2 reduces cardiac fibrosis by attenuating macrophage-mediated inflammation. Cardiovasc Res 2014; 101(3): 383-92.
[http://dx.doi.org/10.1093/cvr/cvt258] [PMID: 24259498]
[112]
Sun J, Axelsson J, Machowska A, et al. Biomarkers of cardiovascular disease and mortality risk in patients with advanced CKD. Clin J Am Soc Nephrol 2016; 11(7): 1163-72.
[http://dx.doi.org/10.2215/CJN.10441015] [PMID: 27281698]
[113]
Carlsson AC, Carrero JJ, Stenvinkel P, et al. High levels of soluble tumor necrosis factor receptors 1 and 2 and their association with mortality in patients undergoing hemodialysis. Cardiorenal Med 2015; 5(2): 89-95.
[http://dx.doi.org/10.1159/000371661] [PMID: 25999957]
[114]
Meuwese CL, Snaedal S, Halbesma N, et al. Trimestral variations of C-reactive protein, interleukin-6 and tumour necrosis factor-α are similarly associated with survival in haemodialysis patients. Nephrol Dial Transplant 2011; 26(4): 1313-8.
[http://dx.doi.org/10.1093/ndt/gfq557] [PMID: 20846939]
[115]
Spoto B, Mattace-Raso F, Sijbrands E, et al. Association of IL-6 and a functional polymorphism in the IL-6 gene with cardiovascular events in patients with CKD. Clin J Am Soc Nephrol 2015; 10(2): 232-40.
[http://dx.doi.org/10.2215/CJN.07000714] [PMID: 25492254]
[116]
Barisione C, Garibaldi S, Ghigliotti G, et al. CD14CD16 monocyte subset levels in heart failure patients. Dis Markers 2010; 28(2): 115-24.
[http://dx.doi.org/10.1155/2010/236405] [PMID: 20364047]
[117]
Wrigley BJ, Shantsila E, Tapp LD, Lip GY. CD14++CD16+ monocytes in patients with acute ischaemic heart failure. Eur J Clin Invest 2013; 43(2): 121-30.
[http://dx.doi.org/10.1111/eci.12023] [PMID: 23240665]
[118]
Amir O, Spivak I, Lavi I, et al. Changes in the monocytic subsets CD14dimCD16+ and CD14++CD16- in chronic systolic heart failure patients. Mediators Inflamm 2012; 2012616384
[http://dx.doi.org/10.1155/2012/616384] [PMID: 23226928]
[119]
Pastori S, Virzì GM, Brocca A, et al. Cardiorenal syndrome type 1: a defective regulation of monocyte apoptosis induced by proinflammatory and proapoptotic factors. Cardiorenal Med 2015; 5(2): 105-15.
[http://dx.doi.org/10.1159/000371898] [PMID: 25999959]
[120]
Virzì GM, Torregrossa R, Cruz DN, et al. Cardiorenal syndrome type 1 may be immunologically mediated: a pilot evaluation of monocyte apoptosis. Cardiorenal Med 2012; 2(1): 33-42.
[http://dx.doi.org/10.1159/000335499] [PMID: 22493601]
[121]
Breglia A, Virzì GM, Pastori S, et al. Determinants of monocyte apoptosis in cardiorenal syndrome type 1. Cardiorenal Med 2018; 8(3): 208-16.
[http://dx.doi.org/10.1159/000488949] [PMID: 29847820]
[122]
Linhart C, Ulrich C, Greinert D, et al. Systemic inflammation in acute cardiorenal syndrome: an observational pilot study. ESC Heart Fail 2018; 5(5): 920-30.
[http://dx.doi.org/10.1002/ehf2.12327] [PMID: 30015388]
[123]
Leuschner F, Panizzi P, Chico-Calero I, et al. Angiotensin-converting enzyme inhibition prevents the release of monocytes from their splenic reservoir in mice with myocardial infarction. Circ Res 2010; 107(11): 1364-73.
[http://dx.doi.org/10.1161/CIRCRESAHA.110.227454] [PMID: 20930148]
[124]
Satoh M, Ishikawa Y, Minami Y, Akatsu T, Nakamura M. Eplerenone inhibits tumour necrosis factor alpha shedding process by tumour necrosis factor alpha converting enzyme in monocytes from patients with congestive heart failure. Heart 2006; 92(7): 979-80.
[http://dx.doi.org/10.1136/hrt.2005.071829] [PMID: 16775109]
[125]
Mizuochi Y, Okajima K, Harada N, et al. Carvedilol, a nonselective beta-blocker, suppresses the production of tumor necrosis factor and tissue factor by inhibiting early growth response factor-1 expression in human monocytes in vitro. Transl Res 2007; 149(4): 223-30.
[http://dx.doi.org/10.1016/j.trsl.2006.11.008] [PMID: 17383596]
[126]
Heymans S, Hirsch E, Anker SD, et al. Inflammation as a therapeutic target in heart failure? A scientific statement from the translational research committee of the heart failure association of the European Society of Cardiology. Eur J Heart Fail 2009; 11(2): 119-29.
[http://dx.doi.org/10.1093/eurjhf/hfn043] [PMID: 19168509]
[127]
Wilk E, Kalippke K, Buyny S, Schmidt RE, Jacobs R. New aspects of NK cell subset identification and inference of NK cells’ regulatory capacity by assessing functional and genomic profiles. Immunobiology 2008; 213(3-4): 271-83.
[http://dx.doi.org/10.1016/j.imbio.2007.10.012] [PMID: 18406373]
[128]
Fu B, Wang F, Sun R, Ling B, Tian Z, Wei H. CD11b and CD27 reflect distinct population and functional specialization in human natural killer cells. Immunology 2011; 133(3): 350-9.
[http://dx.doi.org/10.1111/j.1365-2567.2011.03446.x] [PMID: 21506999]
[129]
Michel T, Poli A, Cuapio A, et al. Human CD56bright NK Cells: An Update. J Immunol 2016; 196(7): 2923-31.
[http://dx.doi.org/10.4049/jimmunol.1502570] [PMID: 26994304]
[130]
Brennan PJ, Brigl M, Brenner MB. Invariant natural killer T cells: an innate activation scheme linked to diverse effector functions. Nat Rev Immunol 2013; 13(2): 101-17.
[http://dx.doi.org/10.1038/nri3369] [PMID: 23334244]
[131]
Van Kaer L, Parekh VV, Wu L. Invariant natural killer T cells: bridging innate and adaptive immunity. Cell Tissue Res 2011; 343(1): 43-55.
[http://dx.doi.org/10.1007/s00441-010-1023-3] [PMID: 20734065]
[132]
Lameris R, de Bruin RC, van Bergen En Henegouwen PM, et al. Generation and characterization of CD1d-specific single-domain antibodies with distinct functional features. Immunology 2016; 149(1): 111-21.
[http://dx.doi.org/10.1111/imm.12635] [PMID: 27312006]
[133]
Getz GS, Reardon CA. Natural killer T cells in atherosclerosis. Nat Rev Cardiol 2017; 14(5): 304-14.
[http://dx.doi.org/10.1038/nrcardio.2017.2] [PMID: 28127028]
[134]
Selathurai A, Deswaerte V, Kanellakis P, et al. Natural killer (NK) cells augment atherosclerosis by cytotoxic-dependent mechanisms. Cardiovasc Res 2014; 102(1): 128-37.
[http://dx.doi.org/10.1093/cvr/cvu016] [PMID: 24469537]
[135]
Whitman SC, Rateri DL, Szilvassy SJ, Yokoyama W, Daugherty A. Depletion of natural killer cell function decreases atherosclerosis in low-density lipoprotein receptor null mice. Arterioscler Thromb Vasc Biol 2004; 24(6): 1049-54.
[http://dx.doi.org/10.1161/01.ATV.0000124923.95545.2c] [PMID: 14988092]
[136]
Hak Ł, Myśliwska J, Więckiewicz J, et al. NK cell compartment in patients with coronary heart disease. Immun Ageing 2007; 4: 3.
[http://dx.doi.org/10.1186/1742-4933-4-3] [PMID: 17488493]
[137]
Hou N, Zhao D, Liu Y, et al. Increased expression of T cell immunoglobulin- and mucin domain-containing molecule-3 on natural killer cells in atherogenesis. Atherosclerosis 2012; 222(1): 67-73.
[http://dx.doi.org/10.1016/j.atherosclerosis.2012.02.009] [PMID: 22387059]
[138]
Szymanowski A, Li W, Lundberg A, et al. Soluble Fas ligand is associated with natural killer cell dynamics in coronary artery disease. Atherosclerosis 2014; 233(2): 616-22.
[http://dx.doi.org/10.1016/j.atherosclerosis.2014.01.030] [PMID: 24534457]
[139]
Jonasson L, Backteman K, Ernerudh J. Loss of natural killer cell activity in patients with coronary artery disease. Atherosclerosis 2005; 183(2): 316-21.
[http://dx.doi.org/10.1016/j.atherosclerosis.2005.03.011] [PMID: 15996672]
[140]
Li W, Lidebjer C, Yuan XM, et al. NK cell apoptosis in coronary artery disease: relation to oxidative stress. Atherosclerosis 2008; 199(1): 65-72.
[http://dx.doi.org/10.1016/j.atherosclerosis.2007.10.031] [PMID: 18068708]
[141]
Backteman K, Ernerudh J, Jonasson L. Natural killer (NK) cell deficit in coronary artery disease: no aberrations in phenotype but sustained reduction of NK cells is associated with low-grade inflammation. Clin Exp Immunol 2014; 175(1): 104-12.
[http://dx.doi.org/10.1111/cei.12210] [PMID: 24298947]
[142]
Zuo J, Shan Z, Zhou L, Yu J, Liu X, Gao Y. Increased CD160 expression on circulating natural killer cells in atherogenesis. J Transl Med 2015; 13: 188.
[http://dx.doi.org/10.1186/s12967-015-0564-3] [PMID: 26071079]
[143]
Vredevoe DL, Widawski M, Fonarow GC, Hamilton M, Martínez-Maza O, Gage JR. Interleukin-6 (IL-6) expression and natural killer (NK) cell dysfunction and anergy in heart failure. Am J Cardiol 2004; 93(8): 1007-11.
[http://dx.doi.org/10.1016/j.amjcard.2003.12.054] [PMID: 15081444]
[144]
Ong S, Ligons DL, Barin JG, et al. Natural killer cells limit cardiac inflammation and fibrosis by halting eosinophil infiltration. Am J Pathol 2015; 185(3): 847-61.
[http://dx.doi.org/10.1016/j.ajpath.2014.11.023] [PMID: 25622543]
[145]
Boukouaci W, Lauden L, Siewiera J, et al. Natural killer cell crosstalk with allogeneic human cardiac-derived stem/progenitor cells controls persistence. Cardiovasc Res 2014; 104(2): 290-302.
[http://dx.doi.org/10.1093/cvr/cvu208] [PMID: 25213554]
[146]
van Puijvelde GHM, Kuiper J. NKT cells in cardiovascular diseases. Eur J Pharmacol 2017; 816: 47-57.
[http://dx.doi.org/10.1016/j.ejphar.2017.03.052] [PMID: 28363745]
[147]
Cochain C, Koch M, Chaudhari SM, et al. Cd8+ t cells regulate monopoiesis and circulating ly6c-high monocyte levels in atherosclerosis in mice. Circ Res 2015; 117(3): 244-53.
[http://dx.doi.org/10.1161/CIRCRESAHA.117.304611] [PMID: 25991812]
[148]
Aslanian AM, Chapman HA, Charo IF. Transient role for CD1d-restricted natural killer T cells in the formation of atherosclerotic lesions. Arterioscler Thromb Vasc Biol 2005; 25(3): 628-32.
[http://dx.doi.org/10.1161/01.ATV.0000153046.59370.13] [PMID: 15591216]
[149]
Ström A, Wigren M, Hultgårdh-Nilsson A, et al. Involvement of the CD1d-natural killer T cell pathway in neointima formation after vas-cular injury. Circ Res 2007; 101(8): e83-9.
[http://dx.doi.org/10.1161/CIRCRESAHA.107.160705] [PMID: 17885216]
[150]
Kyriakakis E, Cavallari M, Andert J, et al. Invariant natural killer T cells: linking inflammation and neovascularization in human athero-sclerosis. Eur J Immunol 2010; 40(11): 3268-79.
[http://dx.doi.org/10.1002/eji.201040619] [PMID: 21061446]
[151]
To K, Agrotis A, Besra G, Bobik A, Toh BH. NKT cell subsets mediate differential proatherogenic effects in ApoE-/- mice. Arterioscler Thromb Vasc Biol 2009; 29(5): 671-7.
[http://dx.doi.org/10.1161/ATVBAHA.108.182592] [PMID: 19251589]
[152]
Rogers L, Burchat S, Gage J, et al. Deficiency of invariant V alpha 14 natural killer T cells decreases atherosclerosis in LDL receptor null mice. Cardiovasc Res 2008; 78(1): 167-74.
[http://dx.doi.org/10.1093/cvr/cvn005] [PMID: 18192239]
[153]
Li Y, To K, Kanellakis P, et al. CD4+ natural killer T cells potently augment aortic root atherosclerosis by perforin- and granzyme B-dependent cytotoxicity. Circ Res 2015; 116(2): 245-54.
[http://dx.doi.org/10.1161/CIRCRESAHA.116.304734] [PMID: 25398236]
[154]
Kyaw T, Winship A, Tay C, et al. Cytotoxic and proinflammatory CD8+ T lymphocytes promote development of vulnerable atherosclerotic plaques in apoE-deficient mice. Circulation 2013; 127(9): 1028-39.
[http://dx.doi.org/10.1161/CIRCULATIONAHA.112.001347] [PMID: 23395974]
[155]
van Puijvelde GH, van Wanrooij EJ, Hauer AD, de Vos P, van Berkel TJ, Kuiper J. Effect of natural killer T cell activation on the initiation of atherosclerosis. Thromb Haemost 2009; 102(2): 223-30.
[http://dx.doi.org/10.1160/TH09-01-0020] [PMID: 19652872]
[156]
Subramanian S, Turner MS, Ding Y, et al. Increased levels of invariant natural killer T lymphocytes worsen metabolic abnormalities and atherosclerosis in obese mice. J Lipid Res 2013; 54(10): 2831-41.
[http://dx.doi.org/10.1194/jlr.M041020] [PMID: 23922382]
[157]
Andoh Y, Fujii S, Iwabuchi K, et al. Lower prevalence of circulating natural killer T cells in patients with angina: a potential novel marker for coronary artery disease. Coron Artery Dis 2006; 17(6): 523-8.
[http://dx.doi.org/10.1097/00019501-200609000-00005] [PMID: 16905964]
[158]
Liu LL, Lu JL, Chao PL, Lin LR, Zhang ZY, Yang TC. Lower prevalence of circulating invariant natural killer T (iNKT) cells in patients with acute myocardial infarction undergoing primary coronary stenting. Int Immunopharmacol 2011; 11(4): 480-4.
[http://dx.doi.org/10.1016/j.intimp.2010.12.019] [PMID: 21238619]
[159]
Wang HX, Li WJ, Hou CL, et al. CD1d-dependent natural killer T cells attenuate angiotensin II-induced cardiac remodelling via IL-10 signalling in mice. Cardiovasc Res 2019; 115(1): 83-93.
[http://dx.doi.org/10.1093/cvr/cvy164] [PMID: 29939225]
[160]
Asaka M, Iida H, Izumino K, Sasayama S. Depressed natural killer cell activity in uremia. Evidence for immunosuppressive factor in uremic sera. Nephron 1988; 49(4): 291-5.
[http://dx.doi.org/10.1159/000185078] [PMID: 3261845]
[161]
Vacher-Coponat H, Brunet C, Lyonnet L, et al. Natural killer cell alterations correlate with loss of renal function and dialysis duration in uraemic patients. Nephrol Dial Transplant 2008; 23(4): 1406-14.
[http://dx.doi.org/10.1093/ndt/gfm596] [PMID: 18029366]
[162]
Cala S, Mazuran R, Kordić D. Negative effect of uraemia and cuprophane haemodialysis on natural killer cells. Nephrol Dial Transplant 1990; 5(6): 437-40.
[http://dx.doi.org/10.1093/ndt/5.6.437] [PMID: 2122320]
[163]
Zaoui P, Hakim RM. Natural killer-cell function in hemodialysis patients: effect of the dialysis membrane. Kidney Int 1993; 43(6): 1298-305.
[http://dx.doi.org/10.1038/ki.1993.182] [PMID: 8315942]
[164]
Gascon A, Orfao A, Lerma JL, et al. Antigen phenotype and cytotoxic activity of natural killer cells in hemodialysis patients. Am J Kidney Dis 1996; 27(3): 373-9.
[http://dx.doi.org/10.1016/S0272-6386(96)90360-1] [PMID: 8604706]
[165]
Döring Y, Pawig L, Weber C, Noels H. The CXCL12/CXCR4 chemokine ligand/receptor axis in cardiovascular disease. Front Physiol 2014; 5: 212.
[PMID: 24966838]
[166]
Döring Y, Noels H, van der Vorst EPC, et al. Vascular CXCR4 Limits Atherosclerosis by Maintaining Arterial Integrity: Evidence From Mouse and Human Studies. Circulation 2017; 136(4): 388-403.
[http://dx.doi.org/10.1161/CIRCULATIONAHA.117.027646] [PMID: 28450349]
[167]
Rowinska Z, Koeppel TA, Sanati M, et al. Role of the CX3C chemokine receptor CX3CR1 in the pathogenesis of atherosclerosis after aortic transplantation. PLoS One 2017; 12(2)e0170644
[http://dx.doi.org/10.1371/journal.pone.0170644] [PMID: 28234900]
[168]
Peraldi MN, Berrou J, Métivier F, Toubert A. Natural killer cell dysfunction in uremia: the role of oxidative stress and the effects of dialysis. Blood Purif 2013; 35(Suppl. 2): 14-9.
[http://dx.doi.org/10.1159/000350839] [PMID: 23676830]
[169]
Lin D, Lavender H, Soilleux EJ, O’Callaghan CA. NF-κB regulates MICA gene transcription in endothelial cell through a genetically in-hibitable control site. J Biol Chem 2012; 287(6): 4299-310.
[http://dx.doi.org/10.1074/jbc.M111.282152] [PMID: 22170063]
[170]
Peukert K, Wingender G, Patecki M, et al. Invariant natural killer T cells are depleted in renal impairment and recover after kidney transplantation. Nephrol Dial Transplant 2014; 29(5): 1020-8.
[http://dx.doi.org/10.1093/ndt/gft495] [PMID: 24353323]

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