CD4+CD28null T cells in acute coronary syndrome: lower with ST-elevation myocardial infarction

Sayed, Nehad; Abdel-Rahman, Safaa M.; Esmat, Iman; Nammas, Wail

doi:10.3109/14017431.2015.1088167

Cited by 2 publications

(1 citation statement)

References 16 publications

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“…Recent studies on patients with rheumatoid arthritis (RA) and systemic lupus erythematosus echo these results: expansion of CD4 + CD28 null cells correlates with significantly higher carotid-intima media thickness and lower brachial artery flow-mediated endothelium-dependent dilation [54,77]. Moreover, CD4 + CD28 null cells are also a risk factor for poorer prognostic outcomes in CVD [57,58]. Interestingly, patients with advanced atherosclerotic disease and concurrent elevations in CD4 + CD28 null cells have a worse prognosis; however, there is an inverse relationship between high CD4 + CD28 null cells and first-time coronary events in a population-based cohort [52].…”

Section: Cvdmentioning

confidence: 94%

Accumulation of CD28null Senescent T-Cells Is Associated with Poorer Outcomes in COVID19 Patients

2021

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Coronavirus disease 2019 (COVID-19), a severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes infectious disease, and manifests in a wide range of symptoms from asymptomatic to severe illness and even death. Severity of infection is related to many risk factors, including aging and an array of underlying conditions, such as diabetes, hypertension, chronic obstructive pulmonary disease (COPD), and cancer. It remains poorly understood how these conditions influence the severity of COVID-19. Expansion of the CD28null senescent T-cell populations, a common phenomenon in aging and several chronic inflammatory conditions, is associated with higher morbidity and mortality rates in COVID-19. Here, we summarize the potential mechanisms whereby CD28null cells drive adverse outcomes in disease and predispose patients to devastating COVID-19, and discuss possible treatments for individuals with high counts of CD28null senescent T-cells.

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