Systemic inflammation plays a major role in the alteration of tissues and loss of organ function, by destruction of organ matrix, by deficient or abnormal tissue repair and fibrosis. Despite a significant step-forward in our understanding of the inflammation pathways, the impact of inflammation remains poorly known in situations such as diabetes, obesity, ischemia-reperfusion (acute myocardial infarction or stroke), acute or chronic transplantation rejection. In the context of a new understanding of autoimmunity, contribution of infectious agents specifically from the digestive tract is now considered important in the induction (changes in protein structure becoming antigenic) and chronicity of inflammatory and autoimmune diseases such as rheumatoid arthritis (RA).
Our areas of research focus on the mechanisms of chronicity in the context of chronic inflammatory diseases, taking the clinical example of RA. We have identified the role of IL-17 and Th17 cells in both the local and systemic aspects of the disease. These concepts have allowed the first therapeutic developments targeting IL-17. This translational project focuses on bridges between well characterized cohorts with collections of biological samples, in vitro and in vivo models, and industry. A particular effort is made in the field of biomarkers of heterogeneity of inflammatory diseases and response to biologic response modifiers (interaction with other WP projects).