The role of T cells in the development of cardiovascular disease in HIV-infected patients

Krikke, M.; Lelyveld, S.F.L. van; Tesselaar, Kiki; Arends, J.E.; Hoepelman, I. M.; Visseren, Frank L.J.

doi:10.1016/j.atherosclerosis.2014.08.054

Cited by 20 publications

(23 citation statements)

References 91 publications

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“…In particular, generalized CD4 + T cell activation as well as CD8 + T cell Kovanen, 1998 [106] Higher in CAD patients than in controls. Among CAD patient, higher in AMI than in unstable angina, and higher in unstable than in stable angina 709 CAD; 273 controls Wang, 2011 [115] IgA -Correlation with risk of AMI and sudden death in dyslipidaemic men 135 Kovanen, 1998 [106] Increased in ACS patients compared to controls activation and senescence were shown to correlate positively with subclinical atherosclerosis in HIV-infected individuals treated with an effective anti-retroviral therapy [137].…”

Section: Atherosclerosis and Disorders Of The Immune Systemmentioning

confidence: 99%

“…The drivers of the spectrum of vascular disease in HIV patients are complex and incompletely understood, and appear to involve both medication‐related elements and chronic inflammation with lymphocyte activation secondary to the loss of CD4 + T cells induced by the virus . In particular, generalized CD4 + T cell activation as well as CD8 + T cell activation and senescence were shown to correlate positively with subclinical atherosclerosis in HIV‐infected individuals treated with an effective anti‐retroviral therapy .…”

Section: Introductionmentioning

confidence: 99%

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The role of T and B cells in human atherosclerosis and atherothrombosis

Ammirati

Moroni

Magnoni

et al. 2015

Clinical and Experimental Immunology

139

104

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SummaryFar from being merely a passive cholesterol accumulation within the arterial wall, the development of atherosclerosis is currently known to imply both inflammation and immune effector mechanisms. Adaptive immunity has been implicated in the process of disease initiation and progression interwined with traditional cardiovascular risk factors. Although the body of knowledge regarding the correlation between atherosclerosis and immunity in humans is growing rapidly, a relevant proportion of it derives from studies carried out in animal models of cardiovascular disease (CVD). However, while the mouse is a well-suited model, the results obtained therein are not fully transferrable to the human setting due to intrinsic genomic and environmental differences. In the present review, we will discuss mainly human findings, obtained either by examination of post-mortem and surgical atherosclerotic material or through the analysis of the immunological profile of peripheral blood cells. In particular, we will discuss the findings supporting a pro-atherogenic role of T cell subsets, such as effector memory T cells or the potential protective function of regulatory T cells. Recent studies suggest that traditional T cell-driven B2 cell responses appear to be atherogenic, while innate B1 cells appear to exert a protective action through the secretion of naturally occurring antibodies. The insights into the immune pathogenesis of atherosclerosis can provide new targets in the quest for novel therapeutic targets to abate CVD morbidity and mortality.

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Section: Atherosclerosis and Disorders Of The Immune Systemmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The role of T and B cells in human atherosclerosis and atherothrombosis

Ammirati

Moroni

Magnoni

et al. 2015

Clinical and Experimental Immunology

139

104

View full text Add to dashboard Cite

show abstract

“…These activated T cells are significantly increased in HIV‐infected individuals and correlate with viral load and disease stage . Some studies have shown that T cell and monocyte activation are independently associated with subclinical atherosclerosis in HIV‐infected individuals on ART as measured by carotid intimal medial thickness or carotid artery stiffness . However, other studies have not found a relationship between T‐cell activation and carotid intimal medial thickness or subsequent cardiovascular events in HIV‐infected individuals …”

Section: Introductionmentioning

confidence: 99%

“…23 Some studies have shown that T cell and monocyte activation are independently associated with subclinical atherosclerosis in HIV-infected individuals on ART as measured by carotid intimal medial thickness or carotid artery stiffness. [24][25][26][27][28][29][30][31] However, other studies have not found a relationship between T-cell activation and carotid intimal medial thickness or subsequent cardiovascular events in HIV-infected individuals. 32,33 The vast majority of cardiovascular disease studies in HIVinfected adults have focused on clinical end points or measures of large-vessel (macrovascular) function.…”

mentioning

confidence: 97%

Role of T‐Cell Dysfunction, Inflammation, and Coagulation in Microvascular Disease in HIV

Sinha

Scherzer

et al. 2016

JAHA

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BackgroundCompared to uninfected adults, HIV‐infected adults on antiretroviral therapy are at increased risk of cardiovascular disease. Given the increase in T‐cell dysfunction, inflammation, and coagulation in HIV infection, microvascular dysfunction is thought to contribute to this excess cardiovascular risk. However, the relationships between these variables remain undefined.Methods and ResultsThis was a cross‐sectional study of 358 HIV‐infected adults from the SCOPE cohort. Macrovascular endothelial function was assessed using flow‐mediated dilation of the brachial artery and microvascular function by reactive hyperemia. T‐cell phenotype was determined by flow cytometry. Plasma markers of inflammation (tumor necrosis factor‐α, interleukin‐6, high‐sensitivity C‐reactive protein, sCD14) and coagulation (fibrinogen, D‐dimer) were also measured. In all HIV+ subjects, markers of inflammation (tumor necrosis factor‐α, high‐sensitivity C‐reactive protein), coagulation (D‐dimer) and T‐cell activation (CD8+PD1+, CD4+interferon+cytomegalovirus‐specific) were associated with worse reactive hyperemia after adjusting for traditional cardiovascular risk factors and co‐infections. In treated and suppressed subjects, tumor necrosis factor‐α and CD8+PD1+ cells remained associated with worse reactive hyperemia after adjustment. Compared to the untreated subjects, CD8+PD1+ cells were increased in the virally suppressed group. Reactive hyperemia was predictive of flow‐mediated dilation.Conclusions CD8+PD1+ cells and tumor necrosis factor‐α were associated with microvascular dysfunction in all HIV+ subjects and the treated and suppressed group. Additionally, D‐dimer, high‐sensitivity C‐reactive protein, sCD‐14, and interleukin‐6 were associated with microvascular dysfunction in all HIV+ subjects. Although T‐cell dysfunction, inflammation, and microvascular dysfunction are thought to play a role in cardiovascular disease in HIV, this study is the first to look at which T‐cell and inflammatory markers are associated with microvascular dysfunction in HIV‐infected individuals.

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“…Whether HIV-infected individuals develop accelerated or accentuated atherosclerosis, when compared with the general population, remains controversial [2]. Nevertheless, the HIV-infected population has specific risk factors associated with atherosclerosis, including chronic inflammation and immune activation associated with HIV itself and/or metabolic disturbances, notably, insulin resistance and dyslipidemia, linked to ART use [3][4][5][6]. Identifying cART-treated HIV-infected individuals at higher risk of cardiovascular disease is of great clinical importance, considering their increased cardiovascular risk overall.…”

Section: Introductionmentioning

confidence: 99%