Autoimmune diseases are characterized by an imbalance between regulatory T cells (Treg) and effector T cells (Teff) both in terms of number and function. Our group previously showed that Teff from the site of inflammation (i.e. synovial fluid, SF) of patients affected by Juvenile Idiopathic Arthritis (JIA) are resistant to autologous Treg-mediated suppression irrespective of the source of Tregs (SF or peripheral blood(PB)-derived). However, it is still unclear whether resistance to suppression is an intrinsic characteristic of SF-derived Teff or it is induced/maintained by local pro-inflammatory antigen presenting cells (APC).
