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Immune Clearance of Senescent Cells to Combat Ageing and Chronic Diseases
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The Immune Response Against Human Cytomegalovirus Links Cellular to Systemic Senescence

1
Immunology and Infectious Diseases Program, Division of BioMedical Sciences, Faculty of Medicine, Memorial University of Newfoundland, 300 Prince Philip Drive, St. John’s, NL A1B 3V6, Canada
2
Lady Davis Institute for Medical Research, Jewish General Hospital, Division of Experimental Medicine, McGill University, Montreal, QC H3A 0G4, Canada
*
Author to whom correspondence should be addressed.
Cells 2020, 9(3), 766; https://doi.org/10.3390/cells9030766
Received: 30 January 2020 / Revised: 11 March 2020 / Accepted: 17 March 2020 / Published: 20 March 2020
Aging reflects long-term decline in physiological function and integrity. Changes arise at a variable pace governed by time-dependent and -independent mechanisms that are themselves complex, interdependent and variable. Molecular decay produces inferior cells that eventually dominate over healthy counterparts in tissues they comprise. In a form of biological entropy, progression from molecular through cellular to tissue level degeneration culminates in organ disease or dysfunction, affecting systemic health. To better understand time-independent contributors and their potential modulation, common biophysical bases for key molecular and cellular changes underlying age-related physiological deterioration must be delineated. This review addresses the potential contribution of cytomegalovirus (CMV)-driven T cell proliferation to cellular senescence and immunosenescence. We first describe molecular processes imposing cell cycle arrest, the foundation of cellular senescence, then focus on the unique distribution, phenotype and function of CMV-specific CD8+ T cells in the context of cellular senescence and “inflammaging”. Their features position CMV infection as a pathogenic accelerant of immune cell proliferation underlying immune senescence. In human immunodeficiency virus (HIV) infection, where increased inflammation and exaggerated anti-CMV immune responses accelerate immune senescence, CMV infection has emerged as a major factor in unhealthy aging. Thus, we speculate on mechanistic links between CMV-specific CD8+ T-cell expansion, immune senescence and prevalence of age-related disorders in HIV infection. View Full-Text
Keywords: cytomegalovirus; clonal selection; telomere; senescence; inflammaging cytomegalovirus; clonal selection; telomere; senescence; inflammaging
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J. Heath, J.; D. Grant, M. The Immune Response Against Human Cytomegalovirus Links Cellular to Systemic Senescence. Cells 2020, 9, 766.

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