Monoclonal T-Cell Proliferation and Plaque Instability in Acute Coronary Syndromes

Liuzzo, Giovanna; Goronzy, Jörg J.; Yang, Hongbo; Kopecky, Stephen L.; Holmes, David R.; Frye, Robert L.; Weyand, Cornelia M.

doi:10.1161/01.cir.101.25.2883

Cited by 490 publications

(416 citation statements)

References 38 publications

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“…CD4+CD28– T cells have been found in patients with cerebrovascular and cardiovascular diseases such as acute coronary syndrome27, 31 and stroke 32, 33, 34. Of note, in these patients this proinflammatory cytokine production is upregulated by the costimulatory receptors OX40 and CD137 on circulating CD4+CD28– T cells,25 which were also found to be located in atherosclerotic plaques preferentially accumulating in unstable lesions 35. Consistent with these previous studies, our study showed that, compared with control groups, patients with acute atherothrombotic stroke had a marked increase of CD4+CD28– T cells, validating a derangement of this cell population occurring in the inflammatory process of this disorder.…”

Section: Discussionmentioning

confidence: 99%

Increased Soluble CD137 Levels and CD4+ T‐Cell‐Associated Expression of CD137 in Acute Atherothrombotic Stroke

et al. 2018

Clinical Translational Sci

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As a proinflammatory cytokine, CD137 (4‐1BB, TNFRSF9) is present in membrane‐bound and soluble forms. Increased expression of CD137 was recently found in T cells in human atherosclerotic plaques. However, the exact role of CD137 in ischemic stroke is not clear. In this study we analyzed the protein levels of soluble CD137 (sCD137) and the expression of CD137 on CD4+ T cells in the peripheral blood of patients with acute atherothrombotic stroke by using the cytometry beads array (CBA) and flow cytometry. Within 24 hours of onset, the stroke patients showed elevated levels of sCD137 (2.7 pg/ml) and CD137 expression on CD4+ T cells (4.9 ± 3.2%) compared with normal controls (1.1 pg/ml, P < 0.01; 1.3 ± 1.0%, P < 0.01). Alterations in CD137 expression may enhance ischemia‐induced inflammatory responses via bidirectional signaling and, consequently, aggravate brain injury in early stages of this disorder.

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Section: Discussionmentioning

confidence: 99%

Increased Soluble CD137 Levels and CD4+ T‐Cell‐Associated Expression of CD137 in Acute Atherothrombotic Stroke

et al. 2018

Clinical Translational Sci

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“…However, the higher systemic frequency of activated T lymphocytes in patients with AMI compared with those with stable angina 53,54 suggests that the adaptive immune system is also activated. In particular, CD4 + CD28 null T-effector cells are increased in the peripheral Evidence of inflammation at remote sites-The activation of the immune system after AMI also results in general systemic inflammation, as evidenced by increased plasma levels of inflammatory cytokines, which are positively correlated with adverse outcomes 5 .…”

Section: Acute Myocardial Infarctionmentioning

confidence: 99%

“…However, the higher systemic frequency of activated T lymphocytes in patients with AMI compared with those with stable angina 53,54 suggests that the adaptive immune system is also activated. In particular, CD4 + CD28 null T-effector cells are increased in the peripheral blood of patients after AMI 55 , and release proinflammatory cytokines (such as interferon-γ), activating monocytes and tissue macrophages, with the level of increase positively correlated with the risk of future acute coronary events 56 .…”

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confidence: 99%

Erratum: Inflammatory processes in cardiovascular disease: a route to targeted therapies

Ruparelia¹,

Chai²,

Fisher³

et al. 2017

Nat Rev Cardiol

189

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Inflammatory processes are firmly established as central to the development and complications of cardiovascular diseases. Elevated levels of inflammatory markers have been shown to be predictive of future cardiovascular events. The specific targeting of these processes in experimental models has been shown to attenuate myocardial and arterial injury, reduce disease progression, and promote healing. However, the translation of these observations and the demonstration of clear efficacy in clinical practice have been disappointing. A major limitation might be that tools currently used to measure 'inflammation' are insufficiently precise and do not provide information about disease site, activity, or discriminate between functionally important activation pathways. The challenge, therefore, is to make measures of inflammation that are more meaningful, and which can guide specific targeted therapies. In this Review, we consider the roles of inflammatory processes in the related pathologies of atherosclerosis and acute myocardial infarction (AMI), by providing an evaluation of the known and emerging inflammatory pathways. We highlight contemporary techniques to characterize and quantify inflammation, and consider how they might be used to guide specific treatments. Finally, we discuss emerging opportunities in the field, including current limitations and challenges that are the focus of ongoing study.Inflammation and its failure to resolve are firmly established as central to the development and complications of several cardiovascular diseases [1][2][3] . Elevated levels of markers of inflammation, such as C-reactive protein (CRP) and serum amyloid A (SAA), have been shown to be predictive of future cardiovascular events across a range of clinical settings [4][5][6] . The role of the innate immune system in the pathogenesis of cardiovascular diseases has been an area of particular focus, with the appreciation that targeting innate immune function Correspondence to R.P.C.: robin.choudhury@cardiov.ox.ac.uk. Author contributionsAll the authors researched data for the article, discussed its contents, and wrote, reviewed, and edited the manuscript before submission. Competing interests statementThe authors declare no competing interests. HHS Public AccessAuthor manuscript Nat Rev Cardiol. Author manuscript; available in PMC 2017 September 01. Author Manuscript Author ManuscriptAuthor ManuscriptAuthor Manuscript in experimental models can variously attenuate disease progression and injury, and promote healing [7][8][9][10] .Processes of inflammation contribute to a broad range of cardiovascular diseases; however, in this Review, we consider the roles of inflammatory processes in the related pathologies of atherosclerosis and acute myocardial infarction (AMI), by providing an evaluation of known and emerging inflammatory pathways that are thought to be central to their pathogenesis, and the consequences of their activation. We highlight contemporary techniques to characterize and quantify inflammation, and consider h...

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“…RA joint inflammation, however, does not seem to affect the number of circulating CD4ϩ cells lacking the CD28 molecule. The expansion of this atypical T cell subset is indeed a peculiar and stable feature in a subset of patients with RA, which does not appear to be linked to the degree of disease activity in the joint (2,7,8), and consequently, cannot be considered a reliable marker to monitor treatment response. However, it is intriguing that the expansion of CD4ϩ,CD28Ϫ cells is strongly linked to extraarticular manifestations of RA (7,8).…”

Section: To the Editormentioning

confidence: 99%

“…The expansion of this atypical T cell subset is indeed a peculiar and stable feature in a subset of patients with RA, which does not appear to be linked to the degree of disease activity in the joint (2,7,8), and consequently, cannot be considered a reliable marker to monitor treatment response. However, it is intriguing that the expansion of CD4ϩ,CD28Ϫ cells is strongly linked to extraarticular manifestations of RA (7,8). This T cell subset, in particular, has a potentially deleterious effect on the arterial wall and represents a risk factor for development of atherosclerosis in RA (2).…”

Section: To the Editormentioning

confidence: 99%

Effect of tumor necrosis factor α inhibition on CD28 surface expression on CD4+ T cells

Gerli¹,

Bocci²,

Shoenfeld³

2006

Arthritis & Rheumatism

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Monoclonal T-Cell Proliferation and Plaque Instability in Acute Coronary Syndromes

Cited by 490 publications

References 38 publications

Increased Soluble CD137 Levels and CD4+ T‐Cell‐Associated Expression of CD137 in Acute Atherothrombotic Stroke

Increased Soluble CD137 Levels and CD4+ T‐Cell‐Associated Expression of CD137 in Acute Atherothrombotic Stroke

Erratum: Inflammatory processes in cardiovascular disease: a route to targeted therapies

Effect of tumor necrosis factor α inhibition on CD28 surface expression on CD4+ T cells

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