Recent evidence suggests that ER stress is activated in conditions of chronic inflammation. The protein A20 is an essential inhibitor of NF-B signalling preventing chronic inflammation. We recently generated different A20 tissue-specific knockout mice which all suffer from chronic inflammation in specific disease models. We will use these models to study the complex interplay between chronic inflammation and ER stress, and determine whether and which ER stress pathways are activated in these mice and how ER stress contributes to the observed disease phenotype.