Figure 1.

Pathogenesis of inflammatory arthritis. (a) The SKG model and (b) a model for rheumatoid arthritis (RA) suggested by the skg mouse. As a result of altered thymic selection, the peripheral T-cell repertoire responds to self-antigen with higher affinity compared with the healthy situation, facilitating self-specific activation and population of the periphery with post-activated memory T cells. These T cells produce proinflammatory cytokines and provide efficient help for autoantibody production, but they have limited capacity for infection control. Antigen-presenting dendritic cells (DCs) are activated directly by fungal β-glucans (panel a) or indirectly through T cells or proinflammatory cytokines (panels a and b). ACPA, antibodies to citrullinated protein; CTL, cytotoxic T lymphocyte; EBV, Epstein-Barr virus; IFN, interferon; IL, interleukin; RF, rheumatoid factor; TCR, T-cell receptor; TNF, tumour necrosis factor; WT, wild-type.