Loading Events
This event has passed.

Julien CHERFILS-VICINI – Institut for the Recherche of Cancer and Aging, Nice, France

As we age, senescent cells accumulate in our tissues and alter the normal function of organs. By accumulating, they contribute to pathological ageing by promoting cancer and chronic diseases (pulmonary fibrosis, diabetes, Alzheimer…). Among stresses that trigger cellular senescence, unrelenting shortening of the DNA forming the chromosome extremities appears to play a key role. TRF2, a key telomeric protein that prevents cells to enter senescence, is down regulated during replicative senescence. We recently revealed that TRF2 over-expression in cancer cells (gastric, lung, colorectal, breast cancer among others) leads a non-cell autonomous mechanism favoring angiogenesis (Zizza et al., Nuc. Ac. Res 2019) and preventing the recruitment and the activation of NK cells (Biroccio et al., Nat Cel. Biol 2013; Cherfils-Vicini et al., EMBO 2019) by triggering immunosuppression (MDSC and Tregs) by a TRF2 dependent heparan-sulfate proteoglycans (HSPG) (HS3ST4, VCAN, GPC-6) mechanisms.

Altogether, these data reveal a link between telomere, glycocalyx and immunity. Strikingly, we recently revealed that a strong glycocalyx remodeling of glycocalyx at senescence can confer immune suppressive properties, favoring thus their accumulations within tissues and making a link with lung fibrosis in mouse models. Understanding how these cells accumulate as we age would allow the development of new therapeutic strategies to fight against age-related diseases and cancer.