Fig. 1.

Cell types and cytokines involved in bone loss and arthritis development in different arthritis mouse models. The arthritis development in the streptococcal cell wall-induced arthritis (SCW) model is mediated by synovial fibroblast and innate immune cells as macrophages, γδ T cells and polymorphonuclear cells (PMN). These cells secrete IL-1, IL-6, IL-23 and TNF-α. No bone erosion is observed in this acute joint inflammation model. In the antigen-induced arthritis (AIA) model, macrophages, B cells and T cells are responsible for disease induction. In AIA, the main cytokines involved are IL-17A, IL-23 and TNF-α. In this model, mild (1) to moderate (2) bone erosion can be observed. The AIA flare-up model is driven mainly by antigen-specific memory T cells that activate synoviocytes leading to synovial inflammation within hours followed by joint destruction. The collagen-induced arthritis (CIA) is an erosive polyarthritis model associated with an auto-immune response against cartilage. CIA is mediated by auto-reactive T and B cells directed against type II collagen. B cells can be differentiated in plasma cells that produce auto-antibodies. Immune complex-mediated immune activation and complement play a role in the progression of the disease. In addition, many pro-inflammatory cytokines such as IL-1, IL-6, IL-17A, IL-22, IL-23 and TNF-α play a role in the development and/or progression of CIA. The degree of bone erosion can vary between mild (1) and severe (3)