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. Overall design: 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