Rheumatoid arthritis (RA) is one of the most common autoimmune diseases and is characterized by
uncontrolled inflammation of the synovial tissue, eventually leading to joint destruction. RA is a
complex disease resulting by a combination of genetic and environmental factors. The most
profound genetic association exists within MHC-II genes suggesting that RA pathology is Thelper cell
dependent. One of the strongest environmental risk factors for RA development is cigarette
smoking. We hypothesize that cigarette smoking might influence immune regulation and trigger the
formation of T cell autoreactivity in the lungs of individuals with a susceptible MHCII background.
Our goal is therefore to explore the regional and systemic features of these autoreactive and
regulatory immune cells and their link to RA onset. Altogether, this studie will lead to a better
understanding of the earliest phases in RA development and could pave the path for more effective
immune therapies.