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RESEARCH PAPER / 2024-12-28

A ganglioside-based immune checkpoint enables senescent cells to evade immunosurveillance during aging.

Charlène Iltis, Iryna Moskalevska, Antoine Debiesse, Laetitia Seguin, Christina Fissoun, Ludovic Cervera, Lyvia Moudombi, Maude Ardin, Anthony Ferrari, Coline Eliott, Didier Pisani, Alexandre Ottaviani, Manon Bourinet, Carmelo Luci, Philippe Gual, Gabriela Makulyte, David Bernard, Manon Durandy, Lou C Duret, Tynhinane Hamidouche, Sarah Kunz, Olivier Croce, Clément Delannoy, Yann Guérardel, Fabrice Allain, Paul Hofman, Delphine Benarroch-Popivker, Laurence Bianchini, Berengère Dadone-Montaudie, Estelle Cosson, Julien Guglielmi, Thierry Pourcher, Véronique M Braud, Marina Shkreli, Yves-Marie Pers, Christian Jorgensen, Jean-Marc Brondello, Chloé C Féral, Marie-Cécile Michallet, Eric Gilson, Julien Cherfils-Vicini

Université Côte d'Azur, Centre National de la Recherche Scientifique (CNRS) UMR7284, Institut National de la Santé et de la Recherche Médicale (INSERM) U1081, Institute for Research on Cancer and Aging, Nice (IRCAN), Nice, France. · pubmed

Abstract

Although senescent cells can be eliminated by the immune system, they tend to accumulate with age in various tissues. Here we show that senescent cells can evade immune clearance by natural killer (NK) cells by upregulating the expression of the disialylated ganglioside GD3 at their surface. The increased level of GD3 expression on senescent cells that naturally occurs upon aging in liver, lung, kidney or bones leads to a strong suppression of NK-cell-mediated immunosurveillance. In mice, we found that targeting GD3

The following analysis is generated by AI and may contain errors. It is separate from the authors’ abstract and is not peer review.

Research summary

The paper addresses the mechanism by which senescent cells evade immune clearance, specifically through the upregulation of GD3 ganglioside. This is relevant to longevity research as it explores a potential root cause of cellular senescence and its implications for aging and age-related diseases. However, while the findings are solid and contribute to the understanding of immune evasion in senescence, they do not present a major breakthrough or transformative implications for the field, thus warranting a moderate impact score.

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