The balance between pro- and anti-inflammatory cell types and cytokines dictates arthritic disease development. (a) During inflammation the joint is overwhelmed by an influx of pro-inflammatory cell types. This activates the immune cells such as macrophages already present in the joint and results in a massive increase in pro-inflammatory cytokines, including IL-17, IL-1β, IFNγ and tumour necrosis factor (TNF)α. Even though regulatory cells can be identified in arthritic joints, it is likely that the pro-inflammatory environment is over-powering and so renders these cells unable to suppress. This results in the joint architecture being destroyed and the synovia becoming inflamed. (b) Regulatory cell types that secrete anti-inflammatory cytokines, including IL-10 and transforming growth factor (TGF)β, are in control of the resolution of joint inflammation in a non-autoimmune individual. This prevents the activation of the Th1 response, antibody production, effector B cell commitment and macrophage activation and so precludes damage to the joint architecture. Breg, regulatory B cell; DC, dendritic cell; IFN, interferon; IL, interleukin; iTreg, induced Treg; nTreg, natural Treg; Treg, regulatory T cell.