Chronic inflammatory diseases such as autoimmune and allergic diseases affect an increasing proportion of the population in developed societies. Although some treatments exist that alleviate some symptoms caused by these pathologies, they are usually not curative so that patients require life-long treatments. In many cases, the treatments only reduce the speed of disease progression, and they can be associated with severe side effects. There is therefore an urgent need to better understand the cellular and molecular processes underlying these diseases, in order to better stratify patients, better predict disease evolution, and develop novel therapeutic strategies. During the last 20 years, B cells, a type of immune cells that has the unique capacity to produce antibodies, have emerged as major players in the pathogenesis of these diseases, as most clearly demonstrated by the beneficial effects of B cell-depletion therapy in a fraction of patients suffering for instance from rheumatoid arthritis or multiple sclerosis. However, we still do not understand precisely how B cells contribute to the pathogenesis in these diseases, and why B cell depletion therapy succeeds or fails. Answering these questions shall help to better select patients prone to respond to B cell depletion therapy, and to develop novel B cell-targeted therapies. Noteworthy, it has meanwhile emerged that B cells do not only have pathogenic functions, but can also mediate protective activities in these diseases. The objectives of the project is to characterize pathogenic pro-inflammatory B cells and protective anti-inflammatory B cells in chronic inflammatory diseases in order to be in a position to track these cells in individual patients, and to define how B cell depletion therapy affects their respective abundance.
