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Review
. 2020 Jun 3:17:16.
doi: 10.1186/s12979-020-00187-9. eCollection 2020.

Role of immune cells in the removal of deleterious senescent cells

Abhijit Kale #  1 , Amit Sharma #  2 , Alexandra Stolzing  2   3 , Pierre-Yves Desprez  1   4 , Judith Campisi  1   5
Affiliations
Review

Role of immune cells in the removal of deleterious senescent cells

Abhijit Kale et al. Immun Ageing. .

Abstract

Cellular senescence is an essentially irreversible arrest of cell proliferation coupled to a complex senescence-associated secretory phenotype (SASP). The senescence arrest prevents the development of cancer, and the SASP can promote tissue repair. Recent data suggest that the prolonged presence of senescent cells, and especially the SASP, could be deleterious, and their beneficial effects early in life can become maladaptive such that they drive aging phenotypes and pathologies late in life. It is therefore important to develop strategies to eliminate senescent cells. There are currently under development or approved several immune cell-based therapies for cancer, which could be redesigned to target senescent cells. This review focuses on this possible use of immune cells and discusses how current cell-based therapies could be used for senescent cell removal.

Keywords: Age-related pathology; Cell-based therapy; Cellular senescence; Immune surveillance; Inflammation; Macrophages; Natural killer cells.

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Conflict of interest statement

Competing interestsNone.

Figures

Fig. 1
Fig. 1
a In a normal tissue microenvironment, the diverse populations of cells are healthy. b In response to different stressors, some cells undergo irreversible growth arrest and acquire a senescent phenotype. Senescent cells have an effect on the innate immune system by secreting inflammatory factors that are part of the SASP. The SASP generally promotes the proliferation and polarization of M1 macrophages and the suppression of M2 macrophages. c In response to the amplified inflammatory signals, NK cells are recruited to site(s) containing senescent cells, which express NK activating ligands on their surface. These NKG2D ligands bind to NKG2D receptors present on NK cells leading to the death of senescent cells. d However, some senescent cells have strategies to avoid elimination. For example, they can express inhibitory ligands that bind to NKG2A receptors on NK cells, blocking their killing. The immune evasion of senescent cells can lead to their accumulation in tissues over time and causes age-associated diseases
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