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Perturbation of the T-cell repertoire in patients with unstable angina.
Abstract
Background —Monocytes are constitutively activated in unstable angina (UA), resulting in the production of IL-6 and the upregulation of acute phase proteins. Underlying mechanisms are not understood. To explore whether the production of the potent monocyte activator IFN-γ is altered in UA, we compared cytokine production by T lymphocytes in patients with UA (Braunwald’s class IIIB) and with stable angina (SA). Methods and Results —Peripheral blood lymphocytes were collected at the time of hospitalization and after 2 and 12 weeks. Cytokine-producing CD4 + and CD8 + T cells were quantified by 3-color flow cytometry after stimulation with phorbol myristate acetate and ionomycin. UA was associated with an increased number of CD4 + and CD8 + T cells producing IFN-γ, whereas patients with SA had higher frequencies of IL-2 + and IL-4 + CD4 + T cells. Expansion of the IFN-γ + T-cell population in UA persisted for at least 3 months. Increased production of IFN-γ in UA could be attributed to the expansion of an unusual subset of T cells, CD4 + CD28 null T cells. Conclusions —Patients with UA are characterized by a perturbation of the functional T-cell repertoire with a bias toward IFN-γ production, suggesting that monocyte activation and acute phase responses are consequences of T-cell activation. IFN-γ is produced by CD4 + CD28 null T cells, which are expanded in UA and distinctly low in SA and controls. The emergence of CD4 + CD28 null T cells may result from persistent antigenic stimulation.
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“CD28− T cells are high producers for interferon-γ (IFN-γ), display cytotoxic functions and accumulate in inflammatory lesions [21–26].”
From T-cell aging in rheumatoid arthritis (2014) · cites this paper as [24]
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Cites
The Pathogenesis of Coronary Artery Disease and the Acute Coronary Syndromes
Epstein, F. H., Fuster, V., Badimón, L., Badimón, L., & Chesebro, J. H. (1992) · New England Journal of Medicine · doi:10.1056/nejm199201303260506 · Cited by 3,792
The Pathogenesis of Coronary Artery Disease and the Acute Coronary Syndromes
Epstein, F. H., Fuster, V., Badimón, L., Badimón, J. J., & Chesebro, J. H. (1992) · New England Journal of Medicine · doi:10.1056/nejm199201233260406 · Cited by 2,713
The Prognostic Value of C-Reactive Protein and Serum Amyloid A Protein in Severe Unstable Angina
Liuzzo, G., Biasucci, L. M., Gallimore, J. R., Grillo, R. L., Rebuzzi, A. G., Pepys, M. B., & Maseri, A. (1994) · New England Journal of Medicine · doi:10.1056/nejm199408183310701 · Cited by 2,354
Self-citationvan der Wal, A. C., Becker, A. E., van der Loos, C. M., & Das, P. K. (1994) · Circulation · doi:10.1161/01.cir.89.1.36 · Cited by 1,921
Production of C-reactive protein and risk of coronary events in stable and unstable angina
Haverkate, E., Thompson, S. G., Pyke, S., Gallimore, J. R., & Mark B Pepys Group (1997) · The Lancet · doi:10.1016/s0140-6736(96)07591-5 · Cited by 1,511
Detection of activated T lymphocytes in the human atherosclerotic plaque.
Hansson, G. K., Holm, J., & Jonasson, L. (1989) · PubMed · Cited by 743
Elevated Levels of Interleukin-6 in Unstable Angina
Biasucci, L. M., Vitelli, A., Liuzzo, G., Altamura, S., Caligiuri, G., Monaco, C. G., Rebuzzi, A. G., Ciliberto, G., & Maseri, A. (1996) · Circulation · doi:10.1161/01.cir.94.5.874 · Cited by 738
Self-citationKovanen, P. T., Kaartinen, M., & Paavonen, T. (1995) · Circulation · doi:10.1161/01.cir.92.5.1084 · Cited by 616
Schmidt, D., Goronzy, J. J., & Weyand, C. M. (1996) · Journal of Clinical Investigation · doi:10.1172/jci118638 · Cited by 482
Self-citationMazzone, A., Servi, S. D., Ricevuti, G., Mazzucchelli, I., Fossati, G., Pasotti, D., Bramucci, E., ANGOLI, L., Marsico, F., & Specchia, G. (1993) · Circulation · doi:10.1161/01.cir.88.2.358 · Cited by 333
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Sorted by citations
Items 301–397 of 397
Type 2 Diabetes, Immunity and Cardiovascular Risk: A Complex Relationship
Pedicino, D., Francesca, A., Alessandro, V., Trotta, F., & Liuzzo, G. (2012) · InTech eBooks · doi:10.5772/50611 · Cited by 7
“…population, which is infrequent in healthy young people and slightly expanded in the elderly, has been detected in patients with unstable angina (Liuzzo et al., 1999, 2000); in this population, a percentage of CD4+CD28null T-cells >4%, representing the 90th percentile of distribution in healthy…”
BackgroundSelf-citationAged T cells and cardiovascular disease
Jung, M. K., & Shin, E. (2017) · Cellular and Molecular Immunology · doi:10.1038/cmi.2017.111 · Cited by 7
Wade, N., Stevenson, B., Dunlap, D. S., & Major, A. S. (2009) · Lupus · doi:10.1177/0961203309345785 · Cited by 7
Rheumatoid disease and ischaemic heart disease: Insights from pathophysiology and vascular biology
Bhatia, G. S., Sosin, M. D., Khattak, F., Davis, R., & Lip, G. Y. H. (2005) · International Journal of Cardiology · doi:10.1016/j.ijcard.2004.12.064 · Cited by 7
Atherosclerosis and Rheumatic Diseases
Jandali, M. M. B. (2015) · Rheumatology Current Research · doi:10.4172/2161-1149.1000147 · Cited by 6
“It was suggested that CD4-CD28-, through their unique features (they lack CD-40 receptor, have cytolytic characteristics, and produce INF-y profusely), are responsible of making the atherosclerotic plaque unstable [77].”
BackgroundLiu, S., Zhong, Z., Zhong, W., Weng, R., Liu, J., Gu, X., & Chen, Y. (2020) · BMC Cardiovascular Disorders · doi:10.1186/s12872-020-01538-6 · Cited by 6
“Previous studies have found a higher level of activated T-cells in ACS patients as compared with stable angina patients [5, 6].”
ResultAnti–tumor necrosis factor α therapy in rheumatoid arthritis: Hitting two birds with one stone?
Warrington, K. J. (2004) · Arthritis Care & Research · doi:10.1002/art.20406 · Cited by 6
Heat Shock Protein Release and Naturally Occurring Exogenous Heat Shock Proteins
Frostegård, J., & Pockley, A. G. (2005) · Cambridge University Press eBooks · doi:10.1017/cbo9780511546310.013 · Cited by 6
Adaptive immunity in acute coronary syndromes: chicken or egg?
Libby, P., & Hansson, G. K. (2017) · European Heart Journal · doi:10.1093/eurheartj/ehx743 · Cited by 6
Pieringer, H., & Studnicka-Benke, A. (2012) · QJM · doi:10.1093/qjmed/hcs205 · Cited by 5
Youssef, S. R., & Elsalakawy, W. A. (2020) · Hematology Transfusion and Cell Therapy · doi:10.1016/j.htct.2020.04.010 · Cited by 5
Li, J., Chen, R., Zhou, J., Wang, Y., Zhao, X., Liu, C., Zhou, P., Chen, Y., Song, L., Li, N., et al. (2023) · Thrombosis and Haemostasis · doi:10.1055/s-0043-1777265 · Cited by 5
“23 Furthermore, it has also been reported that activation of local immune cells is induced by local fl ow perturbation in PE.”
BackgroundVendetti, S., Riccomi, A., Sacchi, A., Sciaraffia, E., Gatta, L., Pioli, C., & Magistris, M. T. D. (2007) · Immunology Letters · doi:10.1016/j.imlet.2007.10.003 · Cited by 5
Navarro‐López, F., Francino, A., Serra, A., Enjuto, M., Reverter, J. C., de Anta, T. J., & Betriu, A. (2003) · Revista Española de Cardiología · doi:10.1016/s0300-8932(03)76901-2 · Cited by 5
T-cells in myocardial infarction: Culprit instigators or mere effectors?
Liberale, L., Bonaventura, A., & Montecucco, F. (2018) · World Journal of Cardiology · doi:10.4330/wjc.v10.i10.123 · Cited by 4
Samstag, Y., Bogert, N. V., Wabnitz, G. H., Din, S., Therre, M., Leuschner, F., Katus, H. A., & Konstandin, M. H. (2020) · The Journal of Immunology · doi:10.4049/jimmunol.2000327 · Cited by 5
‘Hot stuff': inflammatory lymphocyte populations in acute coronary syndrome
Brunetti, N. D. (2014) · Cellular and Molecular Immunology · doi:10.1038/cmi.2014.96 · Cited by 4
Elahi, M. M., & Matata, B. M. (2008) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2008.09.038 · Cited by 4
Ponnusamy, T., Venkatachala, S. K., Manjunatha, R., Kakkar, V. V., & Mundkur, L. (2015) · World Journal of Cardiovascular Diseases · doi:10.4236/wjcd.2015.512043 · Cited by 4
Takeda, H., Spatz, M., Ruetzler, C., McCarron, R. M., Becker, K. J., & Hallenbeck, J. M. (2004) · Springer eBooks · doi:10.1007/978-3-662-05426-0_7 · Cited by 4
“Endothelial cells that have been activated by IFN-y (perhaps from CD4+CD28null NK-T cells (Liuzzo et al. 1999)) express MHC class 11 molecules and can serve as antigen-presenting cells (Hughes et al.”
BackgroundHuang, S., Tang, J.-R., Ct, Z., Sun, L., Lf, G., & Sun, M. (2008) · PubMed · Cited by 4
Inflammation in Acute Coronary Syndrome
(2012) · Chettinad Health City Medical Journal · doi:10.36503/chcmj1(1)-03 · Cited by 4
IL-15 and IL-7: keys to dysregulated inflammation in acute coronary syndromes
Nosalski, R., & Guzik, T. J. (2021) · Cardiovascular Research · doi:10.1093/cvr/cvab189 · Cited by 4
Association between Human Blood Proteome and the Risk of Myocardial Infarction
Wang, L., Zhang, W., Fang, Z., Lu, T., Gu, Z., Sun, T., Han, D. H., Wang, Y., & Cao, F. (2024) · Reviews in Cardiovascular Medicine · doi:10.31083/j.rcm2506199 · Cited by 3
“In patients with rheumatoid vasculitis [58] and acute coronary syndrome [59], CD4+CD28-T cells expressing KIR2DS2 in the absence of opposing inhibitory receptors may promote the activation of autoreactive T cells linked to the mechanisms responsible for the instability of atherosclerotic plaques…”
BackgroundBest practices in mouse models of skin transplantation
Borges, T. J., Krummey, S. M., & Ford, M. L. (2025) · American Journal of Transplantation · doi:10.1016/j.ajt.2025.09.025 · Cited by 4
CD57-Expressing Lymphocytes: From Chronic Viral Response to Age-Related Inflammation
Vallejo-Bermúdez, I. M., Miranda-Echagüe, M. R., Fernández-Álvarez, S., Reina-Alfonso, I., Blanca-Pariente, L., Batista-Duharte, A., & Pera, A. (2026) · Cells · doi:10.3390/cells15050403 · Cited by 3
“In patients with unstable angina pectoris, an increase in CD28nullINF γ + CD4 + T lymphocytes was observed compared to patients with stable angina pectoris and healthy patients [148].”
T Cell Receptor Repertoires Across the Continuum of Vascular, Myocardial, and Age‐Related Diseases
Richter, L., Dias-Ferreira, J., Ramos, G. C., & Ashour, D. (2026) · Immunological Reviews · doi:10.1111/imr.70125 · Cited by 3
“Similarly, IFN-γ producing CD4 + CD28 − T cells are expanded in patients with unstable angina relative to stable angina [201].”
Positron Emission Tomography in Acute Coronary Syndromes
Galiuto, L., Paraggio, L., Caterina, A. R. D., Fedele, E., Locorotondo, G., Leccisotti, L., Giordano, A., Rebuzzi, A. G., & Crea, F. (2011) · Journal of Cardiovascular Translational Research · doi:10.1007/s12265-011-9332-9 · Cited by 3
Masztalewicz, M., Nowacki, P., Bajer‐Czajkowska, A., Kotfis, K., Biernawska, J., Safranow, K., Żukowski, M., & Gutowski, P. (2013) · Folia Neuropathologica · doi:10.5114/fn.2013.37710 · Cited by 3
“Research on patients with coronary arterial diseases indicates that the described cells play a vital role in the process of coronary artery plaque destabilization and acute coronary syndrome occurrence [11-13].”
BackgroundΛιούλιος, Γ., Fylaktou, A., Xochelli, A., Tourountzis, T., Christodoulou, M., Moysidou, E., Stai, S., Vagiotas, L., & Stangou, M. J. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms252010925 · Cited by 2
The Role of Inflammation in Acute Coronary Syndromes Based on Coronary Atherosclerosis
Zhao, P. (2023) · Advances in Clinical Medicine · doi:10.12677/acm.2023.13102144 · Cited by 2
“与一些内源性抑制剂如基质金属蛋白酶组织抑制剂(TIMPS)或胱抑素的平衡。所以若这些活化的蛋白酶增 多或者其抑制剂的减少都可以加快粥样斑块细胞外基质的分解[26]。 适应性免疫在冠状动脉斑块不稳定时也出现改变[27]。此时 ACS 患者的 CD4+T 细胞数量上升,所表 现的特点是细胞表面的共刺激分子 CD28 表达降低,而 CD28 在决定 T 细胞识别抗原的结果中起到了枢纽 作用[28]。此外,ACS 还明显干扰了循环中另外两类 T 细胞的数目,包括 17 型辅助 T 细胞(Th17)及CD4CD25 调节性 T 细胞(Treg)。但是,一些动物的基础研究支持了 IL-17 的促动脉粥样硬化作用,这导致了白细胞介 素-17 (…”
Athérosclérose et connectivites
Meyer, O. (2001) · Revue du Rhumatisme · doi:10.1016/s1169-8330(01)00210-1 · Cited by 2
Collagen Vascular and Infectious Diseases
Agarwal, S., Mohr, J. P., & Elkind, M. S. V. (2011) · Elsevier eBooks · doi:10.1016/b978-1-4160-5478-8.10034-x · Cited by 2
Dichotomous roles of co-stimulatory molecules in diabetes mellitus
Zhong, J., Chen, J., Rao, X., & Duan, L. (2017) · Oncotarget · doi:10.18632/oncotarget.23102 · Cited by 2
Diversity of CD28null T Cells in the Elderly: A Glimpse in a Biological Adaptation of Aging
Griffin, P. C., Michel, J. J., & Vallejo, A. N. (2017) · Springer eBooks · doi:10.1007/978-3-319-64597-1_87-1 · Cited by 2
The Role of Lymphocytes in the Pathogenesis of Atherosclerosis: Focus on CD4+ T Cell Subsets
Dumitriu, I. E., & Kaski, J. C. (2013) · Springer eBooks · doi:10.1007/978-1-4471-4429-8_2 · Cited by 2
Patel, D. R., Gorelik, G. J., & Richardson, B. (2016) · Lupus Open Access · doi:10.35248/2684-1630.16.1.120 · Cited by 2
Non-organ Specific Autoimmunity Involvement in Cardiovascular Disease
Riboldi, P., Gerosa, M., Tincani, A., & Meroni, P. L. (2003) · Technical report · doi:10.1016/s1571-5078(03)01003-1 · Cited by 2
Zal, B., BABOONIAN, C., & Kaski, J. C. (2007) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/01.atv.0000254856.95617.38 · Cited by 2
Andersson, S. H. A., Chalou, A., Mulholland, M., Katra, P., Ljungcrantz, I., Andersson, L. I. M., Engström, G., Nilsson, J. Å., Șchiopu, A., Björkbacka, H., et al. (2025) · European Heart Journal Open · doi:10.1093/ehjopen/oeaf167 · Cited by 1
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Clara, S. (2012) · InTech eBooks · doi:10.5772/25537 · Cited by 1
“In fact, patients with atherosclerosis and acute coronary syndromes exhibit T-cell activation and increased IFN serum levels (Liuzzo et al. 1999) and there is evidence that fibrates, drugs that are PPAR agonists, are anti-inflammatory mediators because they limit inflammatory cytokine expression of…”
BackgroundVascular effects of circulating CD4-T cells in patients with unstable angina
Tousoulis, D., Tourikis, P., Παπαγεωργίου, Ν., Siasos, G., Papaioannou, S., Hatzis, G., Oikonomou, E. K., Toutouzas, K., Synetos, A. G., & Stefanadis, C. (2014) · International Journal of Cardiology · doi:10.1016/j.ijcard.2014.07.044 · Cited by 1
Ratković, N., Dinčić, D., Gligić, B., Vukotić, S., Jovelic, A., & Obradovic, S. D. (2012) · Vojnosanitetski pregled · doi:10.2298/vsp110302010r · Cited by 1
“79 single vessel 11 (50) 8 (62) two vessel 6 (27) 3 (23) three vessel 5 (23) 2 (15) collaterals 0 0 The degree of stenosis of the infarct related artery (%),x ± SD 86 ± 6 47 ± 27 < 0.”
Tratar, G. (2004) · Cited by 1
Kumar, P., Bhargavi, M., Abhilash, T., & Mythili, L. (2016) · International Journal of Medical Research and Review · doi:10.17511/ijmrr.2016.i10.13 · Cited by 1
Rheumatoid arthritis and atherosclerosis: common features in immunopathogenesis. Literature review
Palhuyeva, H. Y., Litvyakov, A. M., & Лагутчев, В. В. (2020) · Vestnik of Vitebsk State Medical University · doi:10.22263/2312-4156.2020.6.31 · Cited by 1
Role of Cytomegalovirus in Driving Cytotoxic CD28null T Cells
Pera, A., Bano, A., & Kern, F. (2019) · Springer eBooks · doi:10.1007/978-3-319-99375-1_124 · Cited by 1
Role of Immunosenescence in Coronary Artery Disease
Boag, S. E., Andreano, E., Martin-Ruiz, C. M., & Spyridopoulos, I. (2019) · Springer eBooks · doi:10.1007/978-3-319-99375-1_129 · Cited by 1
Clinical Relevance in Disease States: Heart Failure and Coronary Disease
Alonso‐Arias, R., Marcos-Fernández, R., Iglesias-Escudero, M., & Moro‐García, M. A. (2019) · Springer eBooks · doi:10.1007/978-3-319-99375-1_154 · Cited by 1
Bocanegra-Zamora, F., Espinosa-Bautista, F., Jiménez‐Rodrìguez, G. M., Massó, F., Páez, A., González‐Pacheco, H., Patlán, M., Eid‐Lidt, G., & Amezcua-Guerra, L. M. (2024) · Journal of Vascular Research · doi:10.1159/000541069 · Cited by 1
“The precise mechanism behind CD28 loss remains elusive, though sustained antigenic stimulation has been proposed as a potential cause [14].”
Diversity of CD28null T Cells in the Elderly: A Glimpse in a Biological Adaptation of Aging
Griffin, P. C., Michel, J. J., & Vallejo, A. N. (2019) · Springer eBooks · doi:10.1007/978-3-319-99375-1_87 · Cited by 1
Atherogenesis and Inflammation
Sangiorgi, G., Mauriello, A., Trimarchi, S., Bonanno, E., & Spagnoli, L. G. (2011) · Interventional Cardiology · doi:10.1002/9781444319446.ch2 · Cited by 1
Lunnon, M. W. (2000) · Expert Opinion on Pharmacotherapy · doi:10.1517/14656566.1.7.1469 · Cited by 1
“• the findings of altered T-cell sub-sets [4]”
BackgroundOpportunities for the treatment of inflammation in cardiovascular disease
Crossman, D. C. (2001) · Expert Opinion on Pharmacotherapy · doi:10.1517/14656566.2.11.1751 · Cited by 1
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BackgroundAntibodies against Chlamydia pneumoniae and their relation to lymphocyte population levels
González-Castañeda, C., Pérez-Castrillón, J.-L., Romero-Gómez, M., & Herreros-Fernández, V. (2002) · International Journal of Cardiology · doi:10.1016/s0167-5273(01)00615-5 · Cited by 1
Me, A., Ea, G., Gendy, N. N., Ns, H., & Mm, S. (2012) · Journal für Kardiologie (Krause & Pachernegg GmbH) · Cited by 1
Arnold, C. R., & Grubeck-Loebenstein, B. (2014) · Elsevier eBooks · doi:10.1016/b978-0-12-801238-3.00153-7 · Cited by 1
Khan, S., Dore, P., & Sewell, W. (2006) · The Journal of the Royal College of Physicians of Edinburgh · doi:10.1177/14782715200636020251 · Cited by 1
High-Sensitivity C-Reactive Protein for Risk Assessment in Acute Coronary Syndromes
Biasucci, L. M., & Abbate, A. (2006) · Humana Press eBooks · doi:10.1007/978-1-59745-051-5_17 · Cited by 1
Studies on inflammatory markers in the prediction of coronary heart disease risk
Kervinen, H. (2005) · Työväentutkimus Vuosikirja · Cited by 1
Collagen Vascular and Infectious Diseases
Elkind, M. S. V., & Mohr, J. P. (2004) · Elsevier eBooks · doi:10.1016/b0-44-306600-0/50030-4 · Cited by 1
Unstable Angina is a Mixed Th17 and Th1 Immune DisorderPreprint
Hu, W.-J. (2012) · viXra
Preclinical models of vascular inflammation
Kalmes, H. A., & Toombs, C. F. (2006) · Birkhäuser Basel eBooks · doi:10.1007/978-3-7643-7760-1_7
Unstable Angina is a syndrome correlated to mixed Th17 and Th1 immune disorderPreprint
Hu, W. (2013) · arXiv (Cornell University) · doi:10.48550/arxiv.1311.4968
Autoimmune aspects of accelerated atherosclerosis in rheumatology
Shoenfeld, Y. (2004) · APLAR Journal of Rheumatology · doi:10.1111/j.1479-8077.2004.00095.x
Drechsler, H., Masztalewicz, M., Safranow, K., & Nowacki, P. (2013) · Neurologia i Neurochirurgia Polska · doi:10.5114/ninp.2013.35574
C-reactive protein and coronary instability
Niccoli, G., Graziani, F., Biasucci, L. M., & Crea, F. (2007) · International Journal of Cardiology · doi:10.1016/j.ijcard.2007.07.055
Inflammatory myocardial injury: the role of lymphocytes in atherosclerosis and other heart diseases
Daniels, M. G., Yap, C., Nandurkar, H., MacIsaac, A. I., & Yii, M. Y. (2009) · Journal of Organ Dysfunction · doi:10.3109/17471060701726190
Is there a future role for anti-TNF therapy in cardiovascular disease?
Jacobsson, L., Jovinge, S. V., & Turesson, C. (2007) · Future Rheumatology · doi:10.2217/17460816.2.3.265
“Increased levels of such T cells have been demonstrated in patients with RA [29], especially those with extra-articular RA associated with CVD [30], unstable coronary artery disease and Wegener’s granulomatosis [31].”
BackgroundArtrite Reumatóide e Doenças Cardiovasculares Rheumatoid Arthritis and Cardiovascular Disease
Torigoe, D. Y., & Laurindo, I. M. M. (2006)
Potential use of sFlt-1 and pterin to predict the clinical outcome of cardiovascular disease.
Marks, E. (2015) · UC Research Repository (University of Canterbury) · doi:10.26021/6379
Mechanisms of vascular protection in chronic inflammatory disease
Thornton, C. C. (2014) · Spiral (Imperial College London) · doi:10.25560/26595
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Yu, H. T., Youn, J., Shin, E., Ha, J., Choi, D., Park, S., Choi, C., Lee, J., Chi, H.-S., Park, S., et al. (2015)
Sandberg, W. J. (2008) · NORA - Norwegian Open Research Archives
Bibliography of One Hundred Key Papers
Jd, T., & Crea, F. (2014)
Arthritis, Obesity, Increased Cardiovascular Risk and Disability
Chatterjee, S. (2011) · CRC Press eBooks · doi:10.1201/b10852-11
The Immune System in Acute Coronary Syndrome
Chyu, K., & Shah, P. K. (2011) · Elsevier eBooks · doi:10.1016/b978-1-4160-4927-2.00008-6
Ghimire, G. (2010) · Spiral (Imperial College London) · doi:10.25560/5618
Atherogenesis and Inflammation
Hayat, U., Thondapu, V., Tsay, T., & Barlis, P. (2016) · Interventional Cardiology · doi:10.1002/9781118983652.ch1
INNATE AND ADAPTIVE IMMUNITY: THE FINE LINE
Weyand, C. M., Goronzy, J. J., Liuzzo, G., Kopecky, S. L., Holmes, D. R., & Frye, R. L. (2001)
Self-citationRole of Immunosenescence in Coronary Artery Disease
Boag, S. E., Andreano, E., Martin-Ruiz, C. M., & Spyridopoulos, I. (2017) · Springer eBooks · doi:10.1007/978-3-319-64597-1_129-1
Clinical Relevance in Disease States: Heart Failure and Coronary Disease
Alonso‐Arias, R., Marcos-Fernández, R., Iglesias-Escudero, M., & Moro‐García, M. A. (2017) · Springer eBooks · doi:10.1007/978-3-319-64597-1_154-1
Unstable Angina is a syndrome correlated to Th17 inflammatory disorderPreprint
Hu, W. (2018) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/396267
Role of Cytomegalovirus in Driving Cytotoxic CD28null T Cells
Pera, A., Bano, A., & Kern, F. (2018) · Springer eBooks · doi:10.1007/978-3-319-64597-1_124-1
The Age-Specific Impact of Cellular Immunity on Long-Term Outcome after Acute Coronary Syndrome
Kazem, N., Hofer, F., Koller, L., Hammer, A., Hengstenberg, C., Niessner, A., & Sulzgruber, P. (2020) · Thrombosis and Haemostasis · doi:10.1055/a-1340-2055
Immune Responses in Atherosclerosis and Microvascular Angina
Dumitriu, I. E., & Kaski, J. C. (2013) · Springer eBooks · doi:10.1007/978-1-4471-4838-8_15
Goronzy, J. J., & Weyand, C. M. (2006) · Arthritis & Rheumatism · doi:10.1002/art.22074
Self-citationCrosstalk between lipoproteins and leukocytes
Bazioti, V. (2022) · University of Groningen research database (University of Groningen / Centre for Information Technology) · doi:10.33612/diss.241440465
PRINCIPAIS EVIDÊNCIAS SOBRE DIAGNÓSTICO E INTERVENÇÕES TERAPÊUTICAS DA SÍNDROME CORONARIANA AGUDA
Nogueira, D. R., Melo, G. C. D. C., Silva, I. D. A. C. E., Moreira, L. E. P., Pedrosa, M. D. S. B., Cardinali, M. D. P., Peron, P. L. V., & Piazzi, R. G. (2024) · EPITAYA eBooks · doi:10.47879/ed.ep.2024264p41
Luqmani, R. A. (2001) · The Journal of the Royal College of Physicians of Edinburgh · doi:10.1177/1478271520013104011
Ghaffar, M. K., & Saeed, I. A. H. M. (2025) · Natural and Engineering Sciences · doi:10.28978/nesciences.1759496
“According to studies, patients whose angina is not stable have more CD4+ and CD8+ T cells producing γ -interferon compared to patients whose angina is stable (Liuzzo et al., 1999).”
Yamada, Z., Muraoka, S., Kawazoe, M., Hirose, W., Kono, H., Yasuda, S., Sugihara, T., & Nanki, T. (2024) · Figshare · doi:10.6084/m9.figshare.26707943
Yamada, Z., Muraoka, S., Kawazoe, M., Hirose, W., Kono, H., Yasuda, S., Sugihara, T., & Nanki, T. (2024) · Figshare · doi:10.6084/m9.figshare.26707940
Komuro (2001) · doi:10.1002/1529-0131(200112)44:12
Metadata
- Authors
- Liuzzo, G., Kopecky, S. L., Frye, R. L., Fallon, W. M. O., Maseri, A., Goronzy, J. J., & Weyand, C. M.
- Affiliations
- Università Cattolica del Sacro Cuore (IT)
- From the Departments of Medicine (G.L., S.L.K., R.L.F., J.J.G., C.M.W.) and Biostatistics (W.M.O.), Mayo Clinic, Rochester, Minn; and the Division of Cardiology (A.M.), Catholic University, Rome, Italy.
- Venue
- Circulation
- Published
- 1999-11-23
- Volume
- 100
- Issue
- 21
- Pages
- 2135-2139
- ISSN
- 0009-7322 (ISSN-L)
- 1524-4539
- OpenAlex
- W1976292294
- Cited by
- 398
- References
- 17
- Citations by year
- 2026: 3 · 2025: 5 · 2024: 12 · 2023: 8 · 2022: 12 · 2021: 9 · 2020: 12 · 2019: 13 · 2018: 10 · 2017: 18 · 2016: 17 · 2015: 17 · 2014: 14 · 2013: 16 · 2012: 21
- FWCI
- 5.81
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Circulation (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Keywords
- unstable angina, stable angina, T cell receptor repertoire, interferon-gamma, CD4+CD28- T cells, CD8+ T cells, CD4+ T cells, cytokine production, monocyte activation, acute phase response, interleukin-6, interleukin-2, IL-4
- MeSH terms
- Adult, Aged, Angina, Unstable, Female, Humans, Interferon-gamma, Male, Middle Aged, Monocytes, T-Lymphocytes, CD4 Antigens, CD28 Antigens
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