Systemic manifestations are a hallmark of chronic inflammatory diseases, as for instance bone destruction in inflammatory bowel disease (IBD). Anti-TNF therapy is the first-line of treatment for IBD but despite its efficacy on gut inflammation and bone destruction, it induces psoriatic skin lesions. In addition of serious consequences for patient care, this side effect raises the question of the tissue specificity of the control of inflammatory responses that remains largely unknown. Our aims are to understand the specific response to anti-TNF in the gut, bone and skin focusing on environmental factors and on immune cells particularly IL-17 secreting cells (Th17 and ILC3). We will combine analysis in a murine IBD model mimicking what observed in patients +/- anti-TNF treatment and in IBD patients treated or not with anti-TNF therapy having or not psoriasis. The results will open new clues for improving therapeutic approaches or prognosis markers for anti-TNF paradoxical effects and may impact other chronic diseases in which such effects are also reported.