Evidence for Antigen-Driven T-Cell Response in Unstable Angina

Caligiuri, Giuseppina; Paulsson, Gabrielle; Nicoletti, Antonino; Maseri, Attilio; Hansson, Göran K.

doi:10.1161/01.cir.102.10.1114

Cited by 110 publications

(68 citation statements)

References 29 publications

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“…For instance, both are inflammatory disorders and there is a specific T-cell-generated immune response to certain antigens in both atherosclerosis and TVD that contribute to vascular damage (34,35). In atherosclerosis, antigen-activated T-cell responses are generated toward oxLDL, resulting in increased atherogenesis and plaque degeneration (7,36,37). In TVD, a similar response is generated toward several foreign epitopes in the allograft.…”

Section: Discussionmentioning

confidence: 99%

“…Both CD4ϩ and CD8ϩ T cells accumulate in atherosclerotic and TVD plaques, and there is an antigen-driven T-cell response in patients with unstable angina (6,7). CD8ϩ T cells have been found to localize to the shoulder region of atherosclerotic plaques and have been well associated with plaque rupture, suggesting that the cytotoxic immune response plays a role in decreasing plaque stability (8).…”

mentioning

confidence: 99%

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Granzyme B in Atherosclerosis and Transplant Vascular Disease: Association with Cell Death and Atherosclerotic Disease Severity

et al. 2003

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Apoptosis of intimal cells is an important contributor to the pathogenesis of atherosclerosis and transplant vascular disease (TVD).Since the activated immune response may be a key regulator of apoptosis in these lesions, we used immunohistochemistry to characterize the presence and localization of granzyme B, a major mediator of the cytotoxic immune response, in advanced atherosclerosis and TVD. Formalin-fixed, paraffin-embedded transverse sections from human left anterior descending coronary arteries were cut serially and stained with antibodies specific for granzyme B, smooth muscle ␣-actin, CD68, and CD3. The amount of granzyme B staining was semi-quantitated on a 0 -5؉/5؉ scale. Also, TUNEL staining and in situ hybridization was performed to visualize cells undergoing cellular damage suggestive of apoptosis, and to localize granzyme B mRNA, respectively. Granzyme B localization was similar in both diseases. This protease was absent in arteries with mild atherosclerosis, but was abundant in the intima and media of vessels with advanced atherosclerosis and TVD. Within the intima, granzyme B localized to TUNEL-positive foam cells surrounding lipid-rich atheromas. Staining of serial sections with granzyme B and either smooth muscle ␣-actin, anti-CD68, or anti-CD3 showed that granzyme B localized to smooth muscle cells, macrophages, and T-cells. Further, in situ hybridization for granzyme B mRNA in TVD cases localized its expression to infiltrating leukocytes and not foam cells. In conclusion, the presence of granzyme B in advanced atherosclerotic lesions and TVD is associated with increasing disease severity and cell death. These observations suggest that granzyme B-mediated apoptosis may contribute to the pathogenesis of these diseases.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Granzyme B in Atherosclerosis and Transplant Vascular Disease: Association with Cell Death and Atherosclerotic Disease Severity

et al. 2003

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“…[4][5][6][7] Recently, the association of pathogenic T cells with acute coronary syndrome in humans was addressed. [8][9][10] However, it remains unclear which specific subpopulation of T cells plays a major role in acute coronary syndrome. CD4 1 CD28 null T cells have been reported to contribute to acute coronary syndrome, 11,12 and expansion of CD4 1 CD28 null T cells is strongly associated with the recurrence of acute coronary events.…”

Section: Introductionmentioning

confidence: 99%

Characterization of CD8+CD57+ T cells in patients with acute myocardial infarction

Youn

Lee

et al. 2014

Cell Mol Immunol

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Although T cells are known to be involved in the pathogenesis of coronary artery disease, it is unclear which subpopulation of T cells contributes to pathogenesis in acute myocardial infarction (MI). We studied the immunological characteristics and clinical impact of CD8 1 CD57 1 T cells in acute MI patients. The frequency of CD57 1 cells among CD8 1 T cells was examined in peripheral blood sampled the morning after acute MI events. Interestingly, the frequency of CD57 1 cells in the CD8 1 T-cell population correlated with cardiovascular mortality 6 months after acute MI. The immunological characteristics of CD8 1 CD57 1 T cells were elucidated by surface immunophenotyping, intracellular cytokine staining and flow cytometry. Immunophenotyping revealed that the CD8 1 CD57 1 T cells were activated, senescent T cells with pro-inflammatory and tissue homing properties. Because a high frequency of CD8 1 CD57 1 T cells is associated with short-term cardiovascular mortality in acute MI patients, this specific subset of CD8 1 T cells might contribute to acute coronary events via their pro-inflammatory and high cytotoxic capacities. Identification of a pathogenic CD8 1 T-cell subset expressing CD57 may offer opportunities for the evaluation and management of acute MI.

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“…14,15 Activated T cells in the non-culprit arteries and systemic circulation of patients with unstable angina, 16,17 together with recent demonstrations that serum levels of C-reactive protein (CRP) predicts the risk of myocardial infarction (MI) or stroke better than total and low-density lipoprotein cholesterol levels, 18 help explain why techniques such as thermography to detect foci of plaque inflammation before the development of thrombosis have been developed. 19,20 However, the lack of data on the natural history of such plaques poses problems.…”

Section: Plaque Inflammationmentioning

confidence: 99%

Vulnerable Atherosclerotic Plaque

2003

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Evidence for Antigen-Driven T-Cell Response in Unstable Angina

Abstract: Our findings suggest that the T-cell response observed in UA patients is antigen-driven and directed to antigens contained in the culprit coronary atherosclerotic plaques.

Cited by 110 publications

References 29 publications

Granzyme B in Atherosclerosis and Transplant Vascular Disease: Association with Cell Death and Atherosclerotic Disease Severity

Granzyme B in Atherosclerosis and Transplant Vascular Disease: Association with Cell Death and Atherosclerotic Disease Severity

Characterization of CD8+CD57+ T cells in patients with acute myocardial infarction

Vulnerable Atherosclerotic Plaque

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