Exploratory pathophysiology monocentric study including an initial case-control study, followed by a cohort for cases.~Controls will be siblings of cases with longitudinal follow-up.~Stool samples will be collected simultaneously from the child with JIA, T1DM or IBD (case) and his/her sibling(s) (control):~at the time of diagnosis~two months after diagnosis (for children with inflammatory disease only)~one year after diagnosis (cases and controls)~Tryptase level in plasma will be recorded for the child with JIA, T1DM or IBD (at the time of diagnosis, 2 months and 1 year after diagnosis)
Two types of inflammatory and autoimmune diseases (excluding monogenic diseases) can be distinguished in children: those similar to adult diseases but with an early onset (type 1 diabetes, inflammatory diseases of the gastrointestinal tract, rheumatoid arthritis with anti-CCP antibodies) and those specific to children that are not described in adults (early-onset juvenile idiopathic arthritis with anti-nuclear and anterior uveitis).~The familial and nosological aggregations suggest that these diseases are probably polygenically determined, and result from interactions with the environment. In a singular way, the incidence of adult diseases is increasing while the age of onset is getting earlier; conversely, there is no increase in early-onset juvenile idiopathic arthritis.~On the other hand, the influence of early events that may alter the microbiotic environment is different for different diseases: whereas cesarean section (or early antibiotic therapy) has been shown to increase the risk of JIA and T1DM, it does not seem to change the risk of IBD. We hypothesize that environmental factors, particularly those related to diet and bacterial and fungal digestive microbiota - are different between these disease categories.