Patients With Acute Coronary Syndrome Show Oligoclonal T-Cell Recruitment Within Unstable Plaque

Palma, Raffaele De; Galdo, Francesco Del; Abbate, Gianfranco; Chiariello, Massimo; Calabrò, Raffaele; Forte, L. A.; Cimmino, Giovanni; Papa, Maria Francesca; Russo, Maria Giovanna; Ambrosio, Giuseppe; Giombolini, Claudio; Tritto, Isabella; Notaristefano, Salvatore; Berrino, Liberato; Rossi, Francesco; Golino, Paolo

doi:10.1161/circulationaha.105.537712

Cited by 113 publications

(86 citation statements)

References 34 publications

(52 reference statements)

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“…We verified whether these events could be identified at the molecular levels in the plaque, in which oligoclonal T cell response has recently been documented (35). First, a difference in LC germline sequences frequency was observed in the two populations, with only 2 LC germline sequences in CPS, compared with 55 LC GLS in PBLs ( p ϭ 0.014).…”

Section: Ag-driven Evolution Of B Cells In Coronary Plaquessupporting

confidence: 54%

Antigen-Driven Evolution of B Lymphocytes in Coronary Atherosclerotic Plaques

Burioni

Canducci

Saita

et al. 2009

The Journal of Immunology

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Recent data indicated that adaptive immunity is involved in the process of atherogenesis. Oligoclonal recruitment of T lymphocytes has been described in coronary plaques of patients with acute coronary syndrome. However, the nature of immune response remains to be determined. In the present study, we examined the Ab response in six coronary plaques obtained by endoluminal directional atherectomy. The IgG1/κ-coding gene repertoires of B lymphocytes present in circulating blood and in coronary plaques were cloned and analyzed. In all of the six plaques, we observed 1) a skewed usage of heavy and light IgG1/κ Ab-coding genes, 2) an oligoclonal distribution of VK, JK, and VH, DH, and JH genes with overrepresentation of some rarely used IgG genes, and 3) the unequivocal signs of Ag-driven clonal expansion and evolution of B cells. The data document for the first time the presence of a local Ag-driven clonal evolution of B cells in human atherosclerotic plaques.

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Section: Ag-driven Evolution Of B Cells In Coronary Plaquessupporting

confidence: 54%

Antigen-Driven Evolution of B Lymphocytes in Coronary Atherosclerotic Plaques

Burioni

Canducci

Saita

et al. 2009

The Journal of Immunology

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“…Reaction mixtures conplaque rupture 5,6) . Unstable plaques are characterized by the activation and infiltration of circulating effector T cells with specificity for both autologous and external antigens 7,8) .…”

Section: Quantification Of Sj-trec By Real-time Pcrmentioning

confidence: 99%

Reduced T-Cell Thymic Export Reflected by sj-TREC in Patients with Coronary Artery Disease

Huang

Ding

Lin

et al. 2016

J Atheroscler Thromb

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Aim:Immunologic dysfunction was recently found to be one of the most important mechanisms underlying the initiation and development of atherosclerosis. Thymus involution can contribute to immune disturbance and disequilibrium of T-cell subsets. This study aimed to explore whether recent thymic emigration (RTE) is impaired in patients with coronary artery disease (CAD). Methods: Content of signal-joint T cell receptor excision circles (sj-TREC) in T lymphocytes, a molecular marker of RTE, was assessed among CAD patients and age-matched controls. Monochrome multiplex quantitative PCR method was used to assess the samples' telomere length in order to exclude the potential influence of T cell proliferation on the dilution of sj-TREC. Patients were grouped according to Gensini score (GS) (low, GS 18; intermediate, GS 18 -41; high, GS 41). Ordinary logistic regression models were used to determine potential risk factors for CAD and GS tertiles. Results: Average copy numbers of sj-TREC per 10 6 T lymphocytes among patients with unstable angina, stable angina, and controls were 726 429, 1213 465, and 1795 838, respectively (P 0.001). However, there was no significant difference in telomere length among groups. Moreover, the content of sj-TREC in the high GS group was most significantly reduced than the low GS group (P 0.001). Multivariate logistic regression analysis revealed that lower sj-TREC was independently associated with the progression of CAD (OR 0.44, P 0.001) and higher GS (OR 0.4, P 0.001). Conclusion: Impaired RTE could be partly responsible for CAD development. Mechanisms may be involved in the disturbance of T lymphocyte compartment and interruption of maintained immune tolerance resulting from thymus involution. J Atheroscler Thromb, 2016; 23: 632-643.

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“…Ten days after stimulation with phytohemagglutinin, IL-2, and feeder cells, the specificity of the T-cell cultures (plaque as well as peripheral blood derived) was analyzed by incubating 5ϫ10 4 T cells and 5ϫ10 4 autologous, irradiated PBMCs as APCs for 4 days in T-cell medium either with or without influenza virus (10 tissue culture infectious dose [TCID 50 ] per cell) in 96-well, round-bottom culture plates (Costar). All combinations were analyzed in quadruplicate.…”

Section: T-cell Proliferation Assaysmentioning

confidence: 99%

“…1 In patients with unstable angina and acute myocardial infarction, the numbers of recently activated T cells are significantly increased. 2,3 Furthermore, de Palma et al 4 showed that unstable but not stable coronary atherosclerotic lesions contain oligoclonal populations of T lymphocytes, which shows that antigen-driven activation and proliferation of effector T cells typically occur in unstable plaques.…”

mentioning

confidence: 99%

Selective Expansion of Influenza A Virus–Specific T Cells in Symptomatic Human Carotid Artery Atherosclerotic Plaques

Keller

Meer

Teeling

et al. 2008

Stroke

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Background and Purpose-Evidence is accumulating that infection with influenza A virus contributes to atherothrombotic disease. Vaccination against influenza decreases the risk of atherosclerotic syndromes, indicating that inflammatory mechanisms may be involved. We tested the hypothesis that influenza A virus-specific T cells contribute to atherosclerotic plaque inflammation, which mediates the onset of plaque rupture. Methods-T-cell cultures were generated from atherosclerotic segments and peripheral blood of 30 patients with symptomatic carotid artery disease. The response of plaque and peripheral blood T cells to influenza A virus was analyzed and expressed as a stimulation index (SI). Selective outgrowth of intraplaque influenza A-specific T cells was calculated by the ratio of plaque T cell SI and peripheral blood T cell SI for each patient. Accordingly, the patients were categorized as high-(SI ratio Ն5), intermediate-(5 ϽSI ratio Յ2), and non-(SI ratio Ͻ2) responders. The presence of influenza A virus in the vessel fragments was evaluated by reverse transcription-polymerase chain reaction. Results-High proliferative responses of plaque-derived T cells to influenza

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Patients With Acute Coronary Syndrome Show Oligoclonal T-Cell Recruitment Within Unstable Plaque

Cited by 113 publications

References 34 publications

Antigen-Driven Evolution of B Lymphocytes in Coronary Atherosclerotic Plaques

Antigen-Driven Evolution of B Lymphocytes in Coronary Atherosclerotic Plaques

Reduced T-Cell Thymic Export Reflected by sj-TREC in Patients with Coronary Artery Disease

Selective Expansion of Influenza A Virus–Specific T Cells in Symptomatic Human Carotid Artery Atherosclerotic Plaques

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