Cellular senescence impact on immune cell fate and function

Vicente, Rita; Mausset-Bonnefont, Anne-Laure; Jørgensen, Christian; Louis‐Plence, Pascale; Brondello, Jean-Marc

doi:10.1111/acel.12455

Cited by 126 publications

(126 citation statements)

References 93 publications

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“…It would be interesting to verify whether NK cell number negatively correlates with senescent cell accumulation in aging tissues. Cells of the immune system, including NK cells, display a senescent phenotype with increasing age, a process called immunosenescence . The idea of ameliorate aged tissue functionality by killing senescent cells is supported by different studies …”

Section: Discussionmentioning

confidence: 99%

Senescent cells: Living or dying is a matter of NK cells

Antonangeli

Zingoni

Soriani

et al. 2019

Journal of Leukocyte Biology

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NK cells are lymphocytes of the innate immune system, which are able to deal promptly with stressed cells. Cellular senescence is a cell stress response leading to cell cycle arrest that plays a key role during tissue homeostasis and carcinogenesis. In this review, how senescent cells trigger an immune response and, in particular, the ability of NK cells to recognize and clear senescent cells are discussed. Special attention is given to the NK cell‐mediated clearance of senescent tumor cells. NK cells kill senescent cells through a mechanism involving perforin‐ and granzyme‐containing granule exocytosis, and produce IFN‐γ following senescent cell interaction, leading to hypothesize that NK cell‐mediated immune clearance of senescent cells not only relies on direct killing but also on cytokine production, that in turn can promote macrophage activation. These aspects, as well as the ability of the senescence‐associated secretory phenotype and senescent cell‐produced extracellular vesicles to modulate NK cell effector functions, are described.

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Section: Discussionmentioning

confidence: 99%

Senescent cells: Living or dying is a matter of NK cells

Antonangeli

Zingoni

Soriani

et al. 2019

Journal of Leukocyte Biology

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“…Senescent cells accumulate in various tissues and organs with aging (Campisi, 2005). Senescent cells have been demonstrated to disrupt tissue structure and function through the secretion of pro‐inflammatory cytokines, chemokines, and proteases, a feature termed the senescence‐associated secretory phenotype (Campisi & d'Adda, 2007; Vicente, Mausset‐Bonnefont, Jorgensen, Louis‐Plence, & Brondello, 2016). Recent studies have demonstrated that selectively eliminating senescent cells can attenuate several age‐dependent disorders (Baker et al., 2011; Chang et al., 2016; Roos et al., 2016; Zhu et al., 2015).…”

Section: Discussionmentioning

confidence: 99%

Young plasma reverses age‐dependent alterations in hepatic function through the restoration of autophagy

et al. 2017

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SummaryRecent studies showing the therapeutic effect of young blood on aging‐associated deterioration of organs point to young blood as the solution for clinical problems related to old age. Given that defective autophagy has been implicated in aging and aging‐associated organ injuries, this study was designed to determine the effect of young blood on aging‐induced alterations in hepatic function and underlying mechanisms, with a focus on autophagy. Aged rats (22 months) were treated with pooled plasma (1 ml, intravenously) collected from young (3 months) or aged rats three times per week for 4 weeks, and 3‐methyladenine or wortmannin was used to inhibit young blood‐induced autophagy. Aging was associated with elevated levels of alanine transaminase and aspartate aminotransferase, lipofuscin accumulation, steatosis, fibrosis, and defective liver regeneration after partial hepatectomy, which were significantly attenuated by young plasma injections. Young plasma could also restore aging‐impaired autophagy activity. Inhibition of the young plasma‐restored autophagic activity abrogated the beneficial effect of young plasma against hepatic injury with aging. In vitro, young serum could protect old hepatocytes from senescence, and the antisenescence effect of young serum was abrogated by 3‐methyladenine, wortmannin, or small interfering RNA to autophagy‐related protein 7. Collectively, our data indicate that young plasma could ameliorate age‐dependent alterations in hepatic function partially via the restoration of autophagy.

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“…5 The factors that contribute to acute GVHD are not well understood, although this patient had bidirectional donor-recipient HLA class I and II mismatches which may support immune surveillance of the lung allograft. Abnormally low telomerase activity is associated with impaired immunosurveillance and defective cell-mediated immunity, 6 and this report suggests that loss-of-function mutations in telomerase may reduce the ability to effectively eliminate donor immune cells in lung grafts.…”

Section: Discussionmentioning

confidence: 79%

Acute graft-versus-host disease following lung transplantation in a patient with a novel TERT mutation

Brestoff

Vessoni

Brenner

et al. 2018

Thorax

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Familial pulmonary fibrosis is associated with loss-of-function mutations in telomerase reverse transcriptase (TERT) and short telomeres. Interstitial lung diseases have become the leading indication for lung transplantation in the USA, and recent data indicate that pathogenic mutations in telomerase may cause unfavourable outcomes following lung transplantation. Although a rare occurrence, solid organ transplant recipients who develop acute graft-versus-host disease (GVHD) have very poor survival. This case report describes the detection of a novel mutation in TERT in a patient who had lung transplantation for familial pulmonary fibrosis and died from complications of acute GVHD.

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Cellular senescence impact on immune cell fate and function

Cited by 126 publications

References 93 publications

Senescent cells: Living or dying is a matter of NK cells

Senescent cells: Living or dying is a matter of NK cells

Young plasma reverses age‐dependent alterations in hepatic function through the restoration of autophagy

Acute graft-versus-host disease following lung transplantation in a patient with a novel TERT mutation

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