Immunotherapies for the treatment of RA have directly targeted pro-inflammatory cytokines such as TNFα and IL-17, and others, such as IL-6, through the blockade of the IL-6 receptor (tocilizumab). Agents that deplete subsets of cells such as T cell depleting anti-CD3 antibodies may also be helpful in re-setting the immune response via the induction of Treg. In future it is hoped that cellular therapies will add to the cannon of therapeutic agents to treat RA either through the in vitro expansion of naturally occurring Treg from patients or the in vitro induction of antigen specific Treg. Alternatively, the generation of TolDCs in vitro and transfer back to the patient could result in altering the balance of inflammation towards tolerance via the reduction in T cell activation and cytokine production, the increase in production of anti-inflammatory cytokines and the induction of functional Treg.
