Figure 4.
Role of T-bet in the pathogenesis of rheumatoid arthritis. T-bet-deficient mice are protected from developing passive collagen antibody-induced arthritis. In this model, T-bet expression in DCs is required for disease pathogenesis. T-bet-deficient DCs are not efficient antigen-presenting cells and activate TH1 cells poorly. In the absence of T-bet, DCs produce much less IL-1α and CCL3 and recruit fewer leukocytes to the joints. In contrast, the role of T-bet in CD4+ T cells is less straightforward. In certain models, such as collagen- or proteoglycan-induced arthritis, expression of T-bet and IFN-γ may have an immunomodulatory effect on the development of arthritis by constraining the magnitude of TH17 responses.
Katie Vicari