The Role of IL-1β in the Bone Loss during Rheumatic Diseases

Figure 1

The inflammatory cascade during autoimmune and autoinflammatory diseases leading to bone resorption. Activated T cells produce IL-1β and RANKL. IL-1β stimulates T and B cells in an autocrine and paracrine fashion amplifying the inflammatory response. Macrophages after influence of IL1 and RANKL produce these 2 molecules and transdifferentiate toward preosteoclasts, which activated themselves, display strong homing to the bone, and produced higher levels of IL-1β and RANKL leading to the increased bone resorption.