LINE-1 elements are derepressed in senescent cells and elicit a chronic Type-I Interferon response

It is not known to what extent retrotransposable elements contribute to the development of age-associated diseases. Here we show that during cellular senescence L1s become transcriptionally derepressed and trigger a type-I interferon (IFN-1) response. We propose that RTE activation is an important component of the sterile inflammation that is a hallmark of aging, and that L1 reverse transcriptase is a relevant target for the development of drugs to treat associated disorders. Human normal diploid lung fibroblast cells from proliferative, early senescent and late senescent stages were used to observe relative changes in gene expression and type-I interferon induction